Department of Bioscience & Bioengineering

&ldquo;IIT Jodhpur is committed to impart quality education to facilitate the creation of qualified, competent and responsible human resources to meet the emerging technological challenges of the world. It is working towards creating an equitable learning platform that is positive, accessible and effective in the face of the modern societal and scientific advancements.

Flexibility in curriculum, in all its academic programs, encompassing elements of teaching, research, creativity, innovation and entrepreneurship is the most unique feature of IIT Jodhpur. The Department of Science and Technology (DST), under the National Mission on Cyber Physical Systems, has identified IIT Jodhpur as a Technology &amp; Innovation Hub in the area of Augmented Reality and Virtual Reality. The institute has also been nominated as the coordinator for the Jodhpur City and Knowledge Cluster by the Office of Principal Scientific Adviser, Government of India.

The sprawling 852-acre IIT Jodhpur campus is a majestic tribute to the deep-rooted diverse cultural heritage of the region. The campus is an architectural masterpiece, which is slated to become an international exemplar of sustainability with net-zero energy, and advanced water and waste management strategies.&rdquo;

IIT Jodhpur

Biofilms are consortia of microorganisms encased in extracellular matrix that protect cells from adverse conditions. A biofilm matrix is typically composed of extracellular DNA, cellulose and proteinaceous amyloid fibers. The matrix aids in adhesion to abiotic and biotic surface including medical devices and host tissues. The presence of biofilm makes bacteria more resilient and non-responsive to most current treatment regimes at disposal. Therefore, biofilm-associated infections are serious threat in hospital set-tings and pose a huge burden on economy. Inhibition of matrix components (cellulose and/or amyloid formation) has emerged as a lucrative alternative strategy to cure biofilm-related infections and combat antibiotic resistance. Here we review the current and emerging therapeutic interventions to mitigate persistent infections due to biofilms. The successful implementation of these interventions will have a huge impact on alleviating the current financial burden on healthcare services. © 2020 Bentham Science Publishers.

World University root node

Current Drug Discovery Technologies

Stopping the unstoppable: Unconventional methods to prevent the biofilm growth

Conventional treatments fail to completely eradicate tumor or bacterial infections due to their inherent shortcomings. In recent years, photothermal therapy (PTT) has emerged as an attractive treatment modality that relies on the absorption of photothermal agents (PTAs) at a specific wavelength, thereby transforming the excitation light energy into heat. The advantages of PTT are its high efficacy, specificity, and minimal damage to normal tissues. To this end, various inorganic nanomaterials such as gold nanostructures, carbon nanostructures, and transition metal dichalcogenides have been extensively explored for PTT applications. Subsequently, the focus has shifted to the development of polymeric PTAs, owing to their unique properties such as biodegradability, biocompatibility, non-immunogenicity, and low toxicity when compared to inorganic PTAs. Among various organic PTAs, polyaniline (PANI) is one of the best-known and earliest-reported organic PTAs. Hence, in this review, we cover the recent advances and progress of PANI-based biomaterials for PTT application in tumors and bacterial infections. The future prospects in this exciting area are also addressed. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

Fulltext

Bioengineering

Recent advances of polyaniline-based biomaterials for phototherapeutic treatments of tumors and bacterial infections

Journal of Biomolecular Structure and Dynamics

Structural vaccinology approach to investigate the virulent and secretory proteins of Bacillus anthracis for devising anthrax next-generation vaccine

Chemokines are a sub-group of cytokines that regulate the leukocyte migration. Monocyte chemoattractant protein-1 (MCP/CCL2) is one of the essential CC chemokine that regulates the migration of monocytes into inflamed tissues. It has been observed that the primary sequences of CCL2 orthologs among rodents and primates vary significantly at the C-terminal region. However, no structural details are available for the rodentia family CCL2 proteins. The current study unravelled the structural, dynamics and in-silico functional characteristics of murine CCL2 chemokine using a comprehensive set of NMR spectroscopy techniques and evolutionary approaches. The study unravelled that the N-terminal portion of the murine CCL2 forms a canonical CC chemokine dimer similar to that of human CCL2. However, unlike human CCL2, the murine ortholog exhibits extensive dynamics in the μs-ms timescales. The presence of C-terminal region of the murine CCL2 protein/rodentia family is highly glycosylated, completely disordered, and inhibits the folding of the structured CCL2 regions. Further, it has been observed that the glycosaminoglycan binding surfaces of these orthologs proteins are greatly differed. In a nut shell, this comparative study provided the role of molecular evolution in generating orthologous proteins with differential structural and dynamics characteristics to engage them in specific molecular interactions. © 2020

International Journal of Biological Macromolecules

Dissecting the differential structural and dynamics features of CCL2 chemokine orthologs

Cellular evolution develops several conserved mechanisms by which cells can tolerate various difficult conditions and overall maintain homeostasis. Autophagy is a well-developed and evolutionarily conserved mechanism of catabolism, which endorses the degradation of foreign and endogenous materials via autolysosome. To decrease the burden of the ubiquitin-proteasome system (UPS), autophagy also promotes the selective degradation of proteins in a tightly regulated way to improve the physiological balance of cellular proteostasis that may get perturbed due to the accumulation of misfolded proteins. However, the diverse as well as selective clearance of unwanted materials and regulations of several cellular mechanisms via autophagy is still a critical mystery. Also, the failure of autophagy causes an increase in the accumulation of harmful protein aggregates that may lead to neurodegeneration. Therefore, it is necessary to address this multifactorial threat for in-depth research and develop more effective therapeutic strategies against lethal autophagy alterations. In this paper, we discuss the most relevant and recent reports on autophagy modulations and their impact on neurodegeneration and other complex disorders. We have summarized various pharmacological findings linked with the induction and suppression of autophagy mechanism and their promising preclinical and clinical applications to provide therapeutic solutions against neurodegeneration. The conclusion, key questions, and future prospectives sections summarize fundamental challenges and their possible feasible solutions linked with autophagy mechanism to potentially design an impactful therapeutic niche to treat neurodegenerative diseases and imperfect aging. © 2020 Wiley Periodicals, Inc.

Medicinal Research Reviews

How autophagy can restore proteostasis defects in multiple diseases?

Accumulation of aberrant misfolded proteins is a major hallmark of several neurodegenerative diseases. Intracellular accumulations of such abnormal proteins are selectively cleared by the ubiquitin-proteasome system (UPS). But how the failure of misfolded protein degradation cause proteinopathies is still an unanswered question?. Previous studies have suggested that few selective quality control (QC) E3 ubiquitin ligase from the UPS can selectively target insoluble aggregated proteins for their intracellular degradation. Few reports suggest that lack or aberrant functions of QC E3 ubiquitin ligases can be a possible causative factor of neurodegeneration and aging. Earlier findings indicated that leucine-rich repeat and sterile alpha motif containing-1 (LRSAM1) is associated with Charcot-Marie-Tooth Type 2P (CMT2P) disease in which loss of LRSAM1 function sensitizes peripheral axons for degeneration. Here, our current study for the first time demonstrates that E3 ubiquitin Ligase LRSAM1 is a really interesting new gene (RING) class protein which suppresses the accumulation of misfolded protein aggregates and also alleviates their deleterious cytotoxic effects. We have also observed that LRSAM1 expression is elevated under neurodegenerative stress conditions, and partial depletion of LRSAM1 endogenous levels aggravates mitochondrial abnormalities and severely affects cell survival during proteotoxic insults. Overall, our current finding indicates that LRSAM1 can alleviate cytotoxic insults mediated by a variety of neurodegeneration linked proteotoxic stress events, and most likely LRSAM1 interplay a significant role in between different components of cellular protein quality control mechanism. This study will also allow us to better comprehend the problem of proteinopathies linked with aberrant protein accumulation and open new possibilities to better elucidate the molecular mechanisms involved in the pathologies of neurodegeneration and aging. © 2020 Elsevier Ltd

International Journal of Biochemistry and Cell Biology

Ubiquitin ligase LRSAM1 suppresses neurodegenerative diseases linked aberrant proteins induced cell death

In 1907, Alois Alzheimer observed, as he quoted, development of “numerous fibers” and “adipose saccules” in the brain of his diseased patient Auguste Deter. The neurodegenerative disease became known as Alzheimer’s disease (AD) and is the most common cause of dementia worldwide. AD normally develops with aging and is mostly initiated because of the imbalance between the formation and clearance of amyloid-β (Aβ). Formation of neurofibrillary tangles (NFTs) of hyperphosphorylated tau is another hallmark of AD. Neuroinflammation plays a significant role in the development and pathology of AD. This chapter explores the role of mitochondrial dysfunction in microglia in case of AD. Mitochondrial oxidative stress in microglia has been linked to the development of AD. Elevated generation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential through various mechanisms have been observed in AD. Aβ interacts with microglial receptors, such as triggering receptor expressed in myeloid cells 2 (TREM2), activating downstream pathways causing mitochondrial damage and aggravating inflammation and cytotoxicity. Fibrillar Aβ activates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in microglia leading to elevated induction of mitochondrial ROS which further causes neurotoxicity. Elevated ROS in microglia causes activation of inflammatory and cell death pathways. Production of ATP, regulation of mitochondrial health, autophagy, and mitophagy in microglia play significant roles in the AD pathology. Understanding microglial physiology and mitochondrial dysfunction will enable better therapeutic interventions. © Copyright © 2020 Agrawal and Jha.

Frontiers in Aging Neuroscience

Mitochondrial Dysfunction and Alzheimer’s Disease: Role of Microglia

Recent studies have demonstrated that racial differences can influence breast cancer incidence and survival rate. African American (AA) women are at two to three fold higher risk for breast cancer than other ethnic groups. AA women with aggressive breast cancers show worse prognoses and higher mortality rates relative to Caucasian (CA) women. Over the last few years, effective treatment strategies have reduced mortality from breast cancer. Unfortunately, the breast cancer mortality rate among AA women remains higher compared to their CA counterparts. The focus of this review is to underscore the racial differences and differential regulation/expression of genetic signatures in CA and AA women with breast cancer. Moreover, immune cell infiltration significantly affects the clinical outcome of breast cancer. Here, we have reviewed recent findings on immune cell recruitment in the tumor microenvironment (TME) and documented its association with breast cancer racial disparity. In addition, we have extensively discussed the role of cytokines, chemokines, and other cell signaling molecules among AA and CA breast cancer patients. Furthermore, we have also reviewed the distinct genetic and epigenetic changes in AA and CA patients. Overall, this review article encompasses various molecular and cellular factors associated with breast cancer disparity that affects mortality and clinical outcome. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.

International Journal of Molecular Sciences

Molecular and cellular factors associated with racial disparity in breast cancer

Cancer Research 80 (4 Supplement), P5-04-14-P5-

Abstract P5-04-14: Recombinant Slit2 suppresses breast cancer metastasis by activating anti-tumor macrophages

Detection of eye closing/opening from alpha-blocking in the EEG of occipital region has been used to build human-machine interfaces. This paper presents an alternative method for detection of eye closing/opening from EOG signals in an online setting. The accuracies for correct detection of eye closing and opening operations with the proposed techniques were found to be 95.6% and 91.9% respectively for 8 healthy subjects. These techniques were then combined with the detection of eye blinks, the accuracy of which turned out to be 96.9%. This was then used to build an interface for robotic arm control for a pick and place task. The same task was also carried out using a haptic device as a master. The speed and accuracy for these two methods were then compared to assess quantitatively the ease of using this interface. It appears that the proposed interface will be very useful for persons with neurodegenerative disorders who can perform eye closing/opening and eye blinks. © 2019 Nalecz Institute of Biocybernetics and Biomedical Engineering of the Polish Academy of Sciences