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| 1 | Neural Mechanisms of Mental Fatigue Revisited: New Insights from the Brain Connectome显示文摘Maintaining sustained attention during a prolonged cognitive task often comes at a cost: high levels of mental fatigue. Heuristically, mental fatigue refers to a feeling of tiredness or exhaustion, and a disengagement from the task at hand;it manifests as impaired cognitive and behavioral performance. In order to effectively reduce the undesirable yet preventable consequences of mental fatigue in many real-world workspaces, a better understanding of the underlying neural mechanisms is needed, and continuous efforts have been devoted to this topic. In comparison with conventional univariate approaches, which are widely utilized in fatigue studies, convergent evidence has shown that multivariate functional connectivity analysis may lead to richer information about mental fatigue. In fact, mental fatigue is increasingly thought to be related to the deviated reorganization of functional connectivity among brain regions in recent studies. In addition, graph theoretical analysis has shed new light on quantitatively assessing the reorganization of the brain functional networks that are modulated by mental fatigue. This review article begins with a brief introduction to neuroimaging studies on mental fatigue and the brain connectome, followed by a thorough overview of connectome studies on mental fatigue. Although only a limited number of studies have been published thus far, it is believed that the brain connectome can be a useful approach not only for the elucidation of underlying neural mechanisms in the nascent field of neuroergonomics, but also for the automatic detection and classification of mental fatigue in order to address the prevention of fatigue-related human error in the near future. | Peng Qi Hua Ru Lingyun Gao Xiaobing Zhang Tianshu Zhou Yu Tian Nitish Thakor Anastasios Bezerianos Jinsong Li Yu Sun | 2019 | Engineering2019，5，2： | 5 |
| 2 | The NLRP3 inflammasome: a potential therapeutic target for traumatic brain injury显示文摘Although the precise mechanisms contributing to secondary brain injury following traumatic brain injury are complex and obscure,a number of studies have demonstrated that inflammatory responses are an obvious and early feature in the pathogenesis of traumatic brain injury.Inflammasomes are multiprotein complexes that prompt the stimulation of caspase-1 and subsequently induce the maturation and secretion of proinflammatory cytokines,such as interleukin-1β and interleukin-18.These cytokines play a pivotal role in facilitating innate immune responses and inflammation.Among various inflammasome complexes,the NOD-like receptor family pyrin domain-containing 3(NLRP3)inflammasome is the best characterized,a crucial role for NLRP3 has been demonstrated in various brain diseases,including traumatic brain injury.Several recent studies have revealed the contribution of NLRP3 inflammasome in identifying cellular damage and stimulating inflammatory responses to aseptic tissue injury after traumatic brain injury.Even more important,blocking or inhibiting the activation of the NLRP3 inflammasome may have substantial potential to salvage tissue damage during traumatic brain injury.In this review,we summarize recently described mechanisms that are involved in the activation and regulation of the NLRP3 inflammasome.Moreover,we review the recent investigations on the contribution of the NLRP3 inflammasome in the pathophysiology of TBI,and current advances and challenges in potential NLRP3-targeted therapies.A significant contribution of NLRP3 inflammasome activation to traumatic brain injury implies that therapeutic approaches focused on targeting specific inflammasome components could significantly improve the traumatic brain injury outcomes. | Saifudeen Ismael Heba A.Ahmed Tusita Adris Kehkashan Parveen Parth Thakor Tauheed Ishrat | 2021 | Neural Regeneration Research2021，16，1： | 5 |
| 3 | Antioxidative study of Cerium Oxide nanoparticle functionalised PCL-Gelatin electrospun fibers for wound healing application显示文摘Skin wound healing involves a coordinated cellular response to achieve complete reepithelialisation.Elevated levels of reactive oxygen species(ROS)in the wound environment often pose a hindrance in wound healing resulting in impaired wound healing process.Cerium oxide nanoparticles(CeNPs)have the ability to protect the cells from oxidative damage by actively scavenging the ROS.Furthermore,matrices like nanofibers have also been explored for enhancing wound healing.In the current study CeNP functionalised polycaprolactone(PCL)-gelatin nanofiber(PGNPNF)mesh was fabricated by electrospinning and evaluated for its antioxidative potential.Wide angle XRD analysis of randomly oriented nanofibers revealed^2.6 times reduced crystallinity than pristine PCL which aided in rapid degradation of nanofibers and release of CeNP.However,bioactive composite made between nanoparticles and PCLgelatin maintained the fibrous morphology of PGNPNF upto 14 days.The PGNPNF mesh exhibited a superoxide dismutase(SOD)mimetic activity due to the incorporated CeNPs.The PGNPNF mesh enhanced proliferation of 3T3-L1 cells by^48%as confirmed by alamar blue assay and SEM micrographs of cells grown on the nanofibrous mesh.Furthermore,the PGNPNF mesh scavenged ROS,which was measured by relative DCF intensity and fluorescence microscopy;and subsequently increased the viability and proliferation of cells by three folds as it alleviated the oxidative stress.Overall,the results of this study suggest the potential of CeNP functionalised PCL-gelatin nanofibrous mesh for wound healing applications. | Hilal Ahmad Rather Ria Thakore Ragini Singh Dhwani Jhala Sanjay Singh Rajesh Vasita | 2018 | Bioactive Materials2018，3，2： | 4 |
| 4 | Systems Neuroengineering: Understanding and Interacting with the Brain显示文摘In this paper, we review the current stateof-the-art techniques used for understanding the inner workings of the brain at a systems level. The neural activity that governsour everyday lives involves anintricate coordination of many processes that can be attributed to a variety of brain regions. On the surface, many of these functions can appear to be controlled by speciflc anatomical structures; however, in reality, numerous dynamic networks within the brain contribute to its function through an interconnected web of neuronal and synaptic pathways. The brain, in its healthy or pathological state, can therefore be best understood by taking a systems-level approach. While numerous neuroengineering technologies exist, we focus here on three major thrusts in the field of systems neuroengineering: neuroimaging, neural interfacing, and neuromodulation. Neuroimaging enables us to delineate the structural and functional organization of the brain, which is key in understanding how the neural system functions in both normal and disease states. Based on such knowledge, devices can be used either to communicate with the neural system, as in neural interface systems, or to modulate brain activity, as in neuromodulation systems. The consideration of these three fields is key to the development and application of neuro-devices. Feedback-based neuro-devices require the ability to sense neural activity(via a neuroimaging modality) through a neural interface(invasive or noninvasive) and ultimately to select a set of stimulation parameters in order to alter neural function via a neuromodulation modality. Systems neuroengineering refers to the use of engineering tools and technologies to image, decode, and modulate the brain in order to comprehend its functions and to repair its dysfunction. Interactions between these fields will help to shape the future of systems neuroengineering—to develop neurotechniques for enhancing the understanding of wholebrain function and dysfunction, and the management of neurological and mental disorders. | Bradley J.Edelman Nessa Johnson Abbas Sohrabpour Shanbao Tong Nitish Thakor Bin He | 2015 | Engineering2015，1，3： | 3 |
| 5 | Learning, corporate control and performance requirements in venture capital contracts显示文摘 | Yuk-Shee C Y Siegel D Thakor A | 1990 | International Economic Review1990，31，： | 2 |
| 6 | Role of hepatocellular regeneration in CCl4 autoprotection显示文摘 | Thakore KN Mehendale HM | 1991 | Toxicol Pathol1991，19，1： | 1 |
| 7 | Studies on Biodegradability, Morphology and Thermo-Mechanical Properties of LDPE/Modifided Starch Blends 显示文摘 | Thakore I M Desai S | 2001 | European Polymer Journal2001，37，： | 1 |
| 8 | Adaptive estimation of latency changes in evoked potentials显示文摘 | Kong X Thakor NV | 1996 | IEEE transactions on biomedical engineering1996，43，2： | 1 |
| 9 | Application of adaptive filtering to ECG analysis: Noise cancellation and arrhythmia detection显示文摘 | Thakor N V Zhu Y | 1991 | IEEE Trans on Biomedical Engineering1991，38，8： | 1 |
| 10 | Collateral and Rationing : Sorting Equilibria in Monopolistic and Competitive Credit Markets 显示文摘 | Besanko D A V Thakor | 1987 | International Economic Review1987，28，3： | 1 |
| 11 | Why Do Finns Issue Equity显示文摘 | Amy K Dittmar Anjan V Thakor | 2007 | Journal of Finance2007，62，1： | 1 |
| 12 | Detecting ventricular tachycardia and fibrillation by complexity measure显示文摘 | Zhang Xusheng Zhu Yisheng Thakor N V | 1999 | IEEE Transactions on Biomedical Engineering1999，46，5： | 1 |
| 13 | Why do firms issue equity? 显示文摘 | Dittmar A Thakor A | 2007 | Journal of Finance2007，6，： | 1 |
| 14 | Cometabolic Degradation of Polychlorinated Biphenyls at Low Temperature by Psychrotolerant Bacterium Hydrogenophaga sp. IA3-A显示文摘 | Adewale J. Lambo Thakor R. Patel | 2006 | Current Microbiology2006，，1： | 1 |
| 15 | Counselling of leprosy affected persons and the community 显示文摘 | Thakor HG Murthy PS | 2004 | J Indian Med Assoc2004，102，12： | 1 |
| 16 | Collateral and competitive equilibria with moral hazard and private information显示文摘 | CHAN Y-S THAKOR V | | 0，，2： | 1 |
| 17 | Banking Deregulation: Allocational Consequences or Relaxing Entry Barriers 显示文摘 | Besanko D Thakor A V | 1992 | Journal of Banking and Finance1992，16，5： | 1 |
| 18 | Nonextensive entropy measure of EEG following brain in jury from cardiac arrest显示文摘 | TONG S B ZHU Y S THAKOR N | 2002 | Physiea A2002，305，： | 1 |
| 19 | Banking Deregulation:Allocational Consequences of Relaxing Entry Barriers显示文摘 | Thakor A V | 1992 | Journal of Banking and Finance1992，16，： | 1 |
| 20 | Structure property relationship in polyurethane elastomers containing starch as a crosslinker显示文摘 | THAKORE I M SARAWADE B D | 2000 | Polym Eng Sci2000，40，5： | 1 |
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