A NEW METHOD OF SYNTHESIS OF COENZYME Q10 FROM ISOLATED SOLANESOL FROM TOBACCO WASTE

Objective: Development of new semi-synthetic route for Coenzyme Q10 from solanesol isolated from tobacco waste and structural characterization by FT-IR, 1H & [13]C NMR, LC-MS spectral data and elemental analyses. Methods: The authors described herein a new, short and highly efficient semi-synthetic route for Coenzyme Q10 (Scheme 1,2&3) starting with isolated solanesol (I) from tobacco waste via the formation of solanesol chloride (II), solanesol ester (III), solanesol acetone (IV) and isodecaprenol (V) as an intermediates. Later attachment of two subsections of the target, that is, a benzohydroquinone as an important precursor (VII), and an isodecaprenol (V, 50 carbon chain) was anticipated to occur via a zinc chloride catalyzed coupling reaction obtained Coenzyme Q10 (VI) in 90.00 % isolated yield. The synthesized compounds were characterized by FT-IR, 1H & [13]C NMR, LC-MS spectral data and elemental analyses. Results: Coenzyme Q10 has been semi-synthesized by a novel process from the solanesol isolated from tobacco waste (biological waste) using readily available and inexpensive precursors like PCl3, ethyl acetoacetate, Grignard reagent and benzohydroquinone derivative via the formation of important precursor Isodecaprenol and optimizing the each reaction. The overall yield of Coenzyme Q10 was 17.24% under the optimized conditions. Conclusion: This process achieved CoQ10 starting from an abundantly available solanesol from tobacco waste. Further improvement in the coupling reaction between Isodecaprenol (V) and Benzohydroquinone (VII) in the presence of Lewis acid may lead to a better and viable synthetic process. Hence this process may be economical and potential to be used for large-scale production

Effect of Grain Size on Superplastic Deformation of Metallic Materials

The superplastic deformation exhibited by metals with different grain sizes and their corresponding deformation mechanism influences the industrial metal-forming processes. The coarse-grained materials, which contain grain size greater than 20 μm, exhibited superplastic deformation at high homologous temperature and low strain rate of the order of 10−4 s−1. Fine grain materials (1–20 μm) are generally considered as favorable for superplastic deformation. They possess high-strain-rate sensitivity “m” value, approximately, equal to 0.5 at the temperature of 0.5 times the melting point and at a strain rate of 10−3 to 10−4 s−1. Ultrafine grains (100 nm to less than 1 μm) exhibit superplasticity at high strain rate as well as at low temperature when compared to fine grain materials. It is attributed to the fact that both temperature and strain rates are inversely proportional to the grain size in Arrhenius-type superplastic constitute equation. The superplastic phenomenon with nano-sized grains (10 nm to less than 100 nm) is quite different from their higher-scale counterparts. It exhibits high ductility with high strength. Materials with mixed grain size distribution (bimodal or layered) are found to exhibit superior superplasticity when compared to the homogeneous grain-sized material. The deformation mechanisms governing these superplastic deformations with different scale grain size microstructures are discussed in this chapter

Brain Tumor Prediction using Adaptive Connected Component based GLCM and SVM Method

A crucial stage in the diagnosis of brain disorders using magnetic resonance images is feature extraction. The feature extraction procedure is used to reduce the amount of the picture data by removing the necessary information from the segmented image. The segmentation strategy and features that are extracted have an impact on the classification algorithm's dependability. With the aid of a Support Vector Machine, texture features are retrieved in this study using a Grey Level Co-occurrence Matrix, while form features are extracted using connected areas. Images of benign tumours, malignant tumours, and a normal brain all exhibit distinctive features. The classification of MR images can benefit from this change in feature values. A SVM classifier will receive the features that were thusly obtained for training and testing and further able to classify the abnormalities in brain images

Genetic knockout and pharmacologic inhibition of neuronal nitric oxide synthase attenuate nerve injury-induced mechanical hypersensitivity in mice

Neuronal nitric oxide synthase (nNOS) is a key enzyme for nitric oxide production in neuronal tissues and contributes to the spinal central sensitization in inflammatory pain. However, the role of nNOS in neuropathic pain remains unclear. The present study combined a genetic strategy with a pharmacologic approach to examine the effects of genetic knockout and pharmacologic inhibition of nNOS on neuropathic pain induced by unilateral fifth lumbar spinal nerve injury in mice. In contrast to wildtype mice, nNOS knockout mice failed to display nerve injury-induced mechanical hypersensitivity. Furthermore, either intraperitoneal (100 mg/kg) or intrathecal (30 μg/5 μl) administration of L-NG-nitro-arginine methyl ester, a nonspecific NOS inhibitor, significantly reversed nerve injury-induced mechanical hypersensitivity on day 7 post-nerve injury in wildtype mice. Intrathecal injection of 7-nitroindazole (8.15 μg/5 μl), a selective nNOS inhibitor, also dramatically attenuated nerve injury-induced mechanical hypersensitivity. Western blot analysis showed that the expression of nNOS protein was significantly increased in ipsilateral L5 dorsal root ganglion but not in ipsilateral L5 lumbar spinal cord on day 7 post-nerve injury. The expression of inducible NOS and endothelial NOS proteins was not markedly altered after nerve injury in either the dorsal root ganglion or spinal cord. Our findings suggest that nNOS, especially in the dorsal root ganglion, may participate in the development and/or maintenance of mechanical hypersensitivity after nerve injury

DESIGN AND PERFORMANCE ANALYSIS OF FULL ADDER USING 6-T XOR–XNOR CELL

In this paper, the design and simulation of a high-speed, low power 6-T XOR-XNOR circuit is carried out. Also, the design and simulation of 1-bit hybrid full adder (consisting of 16 transistors) using XOR-XNOR circuit, sum, and carry, is performed to improve the area and speed performance. Its performance is being compared with full adder designs with 20 and 18 transistors, respectively. The performance of the proposed circuits is measured by simulating them in Microwind tool using 180 and 90nm CMOS technology. The performance of the proposed circuit is measured in terms of power, delay, and PDP (Power Delay Product)

Role of spinal cord alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors in complete Freund's adjuvant-induced inflammatory pain

Spinal cord α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) mediate acute spinal processing of nociceptive and non-nociceptive information, but whether and how their activation contributes to the central sensitization that underlies persistent inflammatory pain are still unclear. Here, we examined the role of spinal AMPARs in the development and maintenance of complete Freund's adjuvant (CFA)-induced persistent inflammatory pain. Intrathecal application of two selective non-competitive AMPAR antagonists, CFM-2 (25 and 50 μg) and GYKI 52466 (50 μg), significantly attenuated mechanical and thermal hypersensitivities on the ipsilateral hind paw at 2 and 24 h post-CFA injection. Neither CFM-2 nor GYKI 52466 affected the contralateral basal responses to thermal and mechanical stimuli. Locomotor activity was not altered in any of the drug-treated animals. CFA-induced inflammation did not change total expression or distribution of AMPAR subunits GluR1 and GluR2 in dorsal horn but did alter their subcellular distribution. The amount of GluR2 was markedly increased in the crude cytosolic fraction and decreased in the crude membrane fraction from the ipsilateral L4–5 dorsal horn at 24 h (but not at 2 h) post-CFA injection. Conversely, the level of GluR1 was significantly decreased in the crude cytosolic fraction and increased in the crude membrane fraction from the ipsilateral L4–5 dorsal horn at 24 h (but not at 2 h) post-CFA injection. These findings suggest that spinal AMPARs might participate in the central spinal mechanism of persistent inflammatory pain

Neuropathic pain

Neuropathic pain is caused by a lesion or disease of the somatosensory system, including peripheral fibres (Aβ, Aδ and C fibres) and central neurons, and affects 7-10% of the general population. Multiple causes of neuropathic pain have been described and its incidence is likely to increase owing to the ageing global population, increased incidence of diabetes mellitus and improved survival from cancer after chemotherapy. Indeed, imbalances between excitatory and inhibitory somatosensory signalling, alterations in ion channels and variability in the way that pain messages are modulated in the central nervous system all have been implicated in neuropathic pain. The burden of chronic neuropathic pain seems to be related to the complexity of neuropathic symptoms, poor outcomes and difficult treatment decisions. Importantly, quality of life is impaired in patients with neuropathic pain owing to increased drug prescriptions and visits to health care providers, as well as the morbidity from the pain itself and the inciting disease. Despite challenges, progress in the understanding of the pathophysiology of neuropathic pain is spurring the development of new diagnostic procedures and personalized interventions, which emphasize the need for a multidisciplinary approach to the management of neuropathic pain