A quantum‐based diagnostics approach for additive manufacturing machine

Abstract Current Additive Manufacturing machines have limited techniques to observe process conditions and to decrease process errors. In order to overcome these limitations and increase the level and accuracy of machine intelligence, machine conditions need to be monitored more meticulously. A novel method for the condition monitoring of a 3D‐printer is proposed in this paper. Quantum support vector machine (QSVM) is compiled for recognizing the health condition of the 3D‐printer. The proposed quantum machine learning approach helps in monitoring the health state of the machine and classifies the same as healthy or aberrant. Classical machine learning approaches are inefficient to process the large amount of experimental data in real time. For better decision‐making on such big data, quantum machine learning approaches are deployed which are much more efficient due to their exponential speed and parallel operation on complex sensor data, they show speedups in both the dimensionality and number of experimental data deployed to train the algorithm. The simulation results show that the proposed method has higher accuracy in fault diagnosis than the traditional Support Vector Machine. All the numerical simulations and experiments have been carried out on a real quantum hardware provided by the IBM Quantum computing over the cloud

Astaxanthin Protection against Neuronal Excitotoxicity via Glutamate Receptor Inhibition and Improvement of Mitochondrial Function

Excitotoxicity is known to associate with neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Amyotrophic lateral sclerosis and Huntington’s disease, as well as aging, stroke, trauma, ischemia and epilepsy. Excessive release of glutamate, overactivation of glutamate receptors, calcium overload, mitochondrial dysfunction and excessive reactive oxygen species (ROS) formation are a few of the suggested key mechanisms. Astaxanthin (AST), a carotenoid, is known to act as an antioxidant and protect neurons from excitotoxic injuries. However, the exact molecular mechanism of AST neuroprotection is not clear. Thus, in this study, we investigated the role of AST in neuroprotection in excitotoxicity. We utilized primary cortical neuronal culture and live cell fluorescence imaging for the study. Our results suggest that AST prevents neuronal death, reduces ROS formation and decreases the abnormal mitochondrial membrane depolarization induced by excitotoxic glutamate insult. Additionally, AST modulates intracellular calcium levels by inhibiting peak and irreversible secondary sustained calcium levels in neurons. Furthermore, AST regulates the ionotropic glutamate subtype receptors NMDA, AMPA, KA and mitochondrial calcium. Moreover, AST decreases NMDA and AMPA receptor protein expression levels, while KA remains unaffected. Overall, our results indicate that AST protects neurons from excitotoxic neuronal injury by regulating ionotropic glutamate receptors, cytosolic secondary calcium rise and mitochondrial calcium buffering. Hence, AST could be a promising therapeutic agent against excitotoxic insults in neurodegenerative diseases

Generation of induced pluripotent stem cell line, NIMHi009-A, from PBMCs of an adult healthy male

Human induced pluripotent stem cells provide an exceptional platform for studying pathogenesis in vitro. We, therefore, have generated and characterized human induced pluripotent stem cell (iPSC) line NIMHi009-A derived from peripheral blood mononuclear cells (PBMCs) of healthy adult male control for an epileptic patient carrying voltage gated sodium channel mutation, using Sendai virus-based reprogramming. The generated iPSCs express pluripotency genes and can spontaneously differentiate into three germ layers. These cells display a normal karyotype and are free of mycoplasma. The iPSC line NIMHi009-A can be used as healthy control for modelling various diseases and screening for drugs

Synchronized Ca oscillations in networked hippocampal neurons represent spontaneous glutamatergic synaptic transmission

(A) Network of neurons in mixed hippocampal cultures visualized by Alexa Fluor 594–conjugated Cholera toxin B subunit that binds to ganglioside GM1 on neuronal membrane. (B) TTX (10 nM) sensitive Ca oscillations in a group of neurons. Bath application of 10 μM CNQX (C), 10 μM APV (D), or 1 μM nimodipine inhibited the SCO. For clarity, the data shown in B–D are for five neurons in a field from a typical experiment repeated three to five times. Data in D are mean ± SEM for 30 neurons from three experiments (*, P < 0.005). The controls were taken as SCO in each experiment before drug treatment.<p><b>Copyright information:</b></p><p>Taken from "Nitric Oxide–mediated Modulation of Synaptic Activity by Astrocytic P2Y Receptors"</p><p></p><p>The Journal of General Physiology 2008;132(3):339-349.</p><p>Published online Jan 2008</p><p>PMCID:PMC2518726.</p><p></p

P2Y1 receptors are expressed in smaller neurons with somal diameter ≤ 10 μm (A) but are absent in larger neurons (B)

(C) Inhibition of GABA receptors with 1 μM picrotoxin enhanced the SCO, and application of 100 μM ATP efficiently inhibited the SCO. Data shown are for five neurons in a typical experiment repeated three times. 100 μM ATP (D) or 30 μM UTP (E) induced large [Ca] response in astrocytes that was coincident with SCO inhibition in neurons. The data shown are from neurons and astrocytes in the same field in a typical experiment.<p><b>Copyright information:</b></p><p>Taken from "Nitric Oxide–mediated Modulation of Synaptic Activity by Astrocytic P2Y Receptors"</p><p></p><p>The Journal of General Physiology 2008;132(3):339-349.</p><p>Published online Jan 2008</p><p>PMCID:PMC2518726.</p><p></p

Confocal images of mixed hippocampal cultures immunostained with anti-P2Y receptors (green) and neuronal markers anti-MAP-2 (red)

Both P2Y2 and P2Y4 receptor immunostaining is not seen in neuronal cell bodies or processes but astrocytes are profusely stained. In merged images, some pixels appear yellow because of the neurons (red) overlying the brightly stained (green) astrocytes.<p><b>Copyright information:</b></p><p>Taken from "Nitric Oxide–mediated Modulation of Synaptic Activity by Astrocytic P2Y Receptors"</p><p></p><p>The Journal of General Physiology 2008;132(3):339-349.</p><p>Published online Jan 2008</p><p>PMCID:PMC2518726.</p><p></p