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Human polyglutamine [poly(Q)] disorders such as Huntington's disease, different types of ataxias, etc. are devastating brain illnesses which are characterised by the presence of neurotoxic protein aggregates in the affected neurons. We have recently reported that S6K/4E-BP mediated growth promoting branch of insulin signalling pathway alleviates human poly(Q) induced neurotoxicity in Drosophila disease models. Since, the S6K/4E-BP sub-pathway can be stimulated by various amino acids; we extended our investigation to examine if oral feeding of amino acids delivers rescue against human poly(Q) toxicity in Drosophila. We utilised Drosophila models of two different poly(Q) disorders to test our hypothesis. Glutamine was fed to the test flies orally mixed in the food. Control and treated flies were then tested for different parameters, such as formation of poly(Q) aggregates and neurodegeneration, to evaluate glutamine's proficiency in mitigating poly(Q) neurotoxicity. Our study, for the first time, reports that glutamine feeding stimulates the growth promoting S6K/4E-BP branch of insulin signalling pathway and restricts pathogenesis of poly(Q) disorders in Drosophila disease models. We noted that glutamine treatment restricts the formation of neurotoxic poly(Q) aggregates and minimises neuronal deaths. Further, glutamine treatment re-establishes the chromatin architecture by improving the histone acetylation which is otherwise compromised in poly(Q) expressing neuronal cells. Since, the insulin signalling pathway as well as mechanism of action of glutamine are fairly conserved between human and Drosophila, our finding strongly suggests that glutamine holds immense potential to be developed as an intervention therapy against the incurable human poly(Q) disorders. [ABSTRACT FROM AUTHOR]

Parkinson's disease is the second most common neurodegenerative disease characterized by the loss of dopaminergic neurons in the brain. Parkinson's disease has both familial and sporadic cases of origin governed differentially by genetic and/or environmental factors. Different epidemiological studies have proposed an association between the pathogenesis of cancer and Parkinson's disease; however, a precise correlation between these two illnesses could not be established yet. In this study, we examined the disease-modifying property of dmyc (a Drosophila homolog of human cmyc proto-oncogene) in the paraquat-induced sporadic Parkinson's disease model of Drosophila. We report for the first time that targeted upregulation of dMyc significantly restricts paraquat-mediated neurotoxicity. We observed that paraquat feeding reduces the cellular level of dMyc. We further noted that targeted upregulation of dMyc in paraquat-exposed flies mitigates degeneration of dopaminergic neurons by reinstating the aberrantly activated JNK pathway, and this in turn improves the motor performance and survival rate of the flies. Our study provides the first evidence that improved cellular level of dMyc could efficiently minimize the neurotoxic effects of paraquat, which could be beneficial in designing novel therapeutic strategies against Parkinson's disease. • Paraquat exposure reduces the cellular level of dMyc in Drosophila. • Upregulation of dMyc restricts paraquat-mediated degeneration of dopaminergic neurons in Drosophila. • Upregulation of dMyc improves motor performance and survival of paraquat exposed flies. • Upregulation of dMyc reinstates aberrantly activated JNK pathway to mitigate paraquat-mediated neurotoxicity. [ABSTRACT FROM AUTHOR]

Increasing reports suggest insulin signalling pathway as a putative drug target against polyglutamine [poly(Q)] disorders, such as Huntington's disease (HD), Spinocerebellar ataxias (SCA) 1, 2, 3 etc. However, studies on drug-based stimulation of insulin signalling cascade to mitigate poly(Q) pathogenesis are lacking. In our study, we adopted an evidence-based approach to examine if some established insulin stimulating drug can be utilized to restrict poly(Q) aetiology in Drosophila disease models. For the first time, we report that glipizide, an FDA approved anti-diabetic drug upregulates insulin signalling in poly(Q) expressing tissues and restricts formation of inclusion bodies and neurodegeneration. Moreover, it reinstates the chromatin architecture by improving histone acetylation, which is otherwise abrogated due to poly(Q) toxicity. In view of the functional conservation of insulin signalling pathway in Drosophila and humans, our finding strongly suggests that glipizide can be repurposed as an effective treatment strategy against the neurodegenerative poly(Q) disorders. Also, with appropriate validation studies in mammalian disease models, glipizide could be subsequently considered for the clinical trials in human patients. • Glipizide upregulates insulin signalling in human poly(Q) expressing tissues in Drosophila. • Glipizide restricts formation of poly(Q) aggregates and neurodegeneration. • Glipizide improves histone acetylation and reinstate chromatin architecture in poly(Q) expressing cells. • Glipizide may be repurposed to restrict pathogenesis of human poly(Q) disorders. [ABSTRACT FROM AUTHOR]

An efficient one pot synthesis of various bis-coumarinyl methane derivatives was investigated by condensing a series of aldehydes with 4-hydroxy coumarin in the presence of Amberlyst 15 catalyst under refluxing conditions in ethanol–water (1:1). This one pot domino Knoevenagel condensation/Micheal addition reaction provides excellent yield of bis-coumarinyl methane derivatives with lots of advantages like shorter reaction time, eco-friendly reaction medium, simple work up, recyclability of the catalyst and chromatography-free purification. Moreover, the synthesized compound was exploited to develop bis-coumarinyl methylene-based nanostructured materials of special interests which were investigated by UV–Vis, fluorescence spectroscopy, imaging in scanning electron microscope and atomic force microscope. Our UV–Vis and fluorescence study indicated that some of the organic compounds are organized as H-aggregate in the thin film. We also investigated I–V characteristics of the thin film of some of the selective compounds which showed write-once-read-more memory switching behaviour onto the thin film under investigations. [ABSTRACT FROM AUTHOR]

Neurodegenerative tauopathies such as Alzheimer's and Parkinson's diseases are characterized by hyperphosphorylation of tau protein and their subsequent aggregation in the forms of paired helical filaments and/or neurofibrillary tangles in specific areas of the brain. Despite several attempts, it remains a challenge to develop reliable biomarkers or effective drugs against tauopathies. It is increasingly evident now that due to the involvement of multiple cellular cascades affected by the pathogenic tau molecules, a single genetic modifier or a molecule is unlikely to be efficient enough to provide an inclusive rescue. Hence, multitargets based combinatorial approach(s) have been suggested to provide an efficient rescue against tauopathies. We have reported earlier that targeted downregulation of dmyc (a Drosophila homolog of human cmyc proto‐oncogene) restricts tau etiology by limiting tau hyperphosphorylation and heterochromatin loss. Although, dmyc generates a significant rescue; however, it is not proficient enough to provide a complete alleviation against tauopathies. Here, we report that tissue‐specific concurrent downregulation of dmyc and gsk3β conveys a near‐complete rescue against tau toxicity in Drosophila. We noted that combinatorial downregulation of dmyc and gsk3β reduces tau hyperphosphorylation, restricts the formation of neurofibrillary tangles, and restores heterochromatin loss to the physiological level. Our subsequent investigations revealed that dmyc regulates gsk3β via protein phosphatase 2A (dPP2A) in a dose‐dependent manner to regulate tau pathogenesis. We propose that dmyc and gsk3β candidates can be utilized in a synergistic manner for the development of an efficient combinatorial therapeutic approach against the devastating human tauopathies. [ABSTRACT FROM AUTHOR]

Abstract We theoretically investigate the transport properties of a normal-insulator-superconductor (NIS) junction of silicene in the thin barrier limit. Similar to graphene the tunneling conductance in such NIS structure exhibits an oscillatory behavior as a function of the strength of the barrier in the insulating region. However, unlike in graphene, the tunneling conductance in silicene can be controlled by an external electric field owing to its buckled structure. We also demonstrate the change in behavior of the tunneling conductance across the NIS junction as we change the chemical potential in the normal silicene region. In addition, at high doping levels in the normal region, the period of oscillation of the tunneling conductance as a function of the barrier strength changes from π / 2 to π with the variation of doping in the superconducting region of silicene. Highlights • Tunneling conductance (TC) exhibits contrasting behavior in various doping regimes. • Unlike in graphene, TC in silicene shows strong dependence on electric field. • Electric field acts as a switch to tune the conductance from on to off condition. • Unusual doping dependence of period of oscillation of TC vs the barrier strength. [ABSTRACT FROM AUTHOR]

Tauopathies represent a group of neurodegenerative disorder which are characterized by the presence of tau positive specialized argyrophilic and insoluble intraneuronal and glial fibrillar lesions known as neurofibrillary tangles (NFTs). Tau is a neuron specific microtubule binding protein which is required for the integrity and functioning of neuronal cells, and hyperphosphorylation of tau and its subsequent aggregation and paired helical filaments (PHFs) and NFTs has emerged as one of the major pathogenic mechanisms of tauopathies in human and mammalian model systems. Modeling of human tauopathies in Drosophila results in manifestation of associated phenotypes, and a recent study has demonstrated that similar to human and mammalian models, accumulation of insoluble tau aggregates in the form of typical neurotoxic NFTs triggers the pathogenesis of tauopathies in fly models. In view of the availability of remarkable genetic tools, Drosophila tau models could be extremely useful for in-depth analysis of the role of NFTs in neurodegeneration and tau aetiology, and also for the screening of novel gene(s) and molecule(s) which suppress the toxicity of tau aggregates. [ABSTRACT FROM AUTHOR]

Formation of Neurofibrillary Tangles (NFTs) in neuronal tissues has been implicated as the hallmark of disease pathogenesis and tau mediated toxicity in human and mammalian models. However, previous studies had failed to correlate NFT formation with pathogenesis of human neuronal tauopathies in Drosophila disease models. Though, a recent report suggests formation of tau mediated NFTs like structures confined to dopaminergic neurons in Drosophila adult brain; by utilizing various approaches, we demonstrate distinct and recurrent formation of NFTs in Drosophila neuronal tissues upon expression of wild type or mutant isoforms of human tau protein, and this appears as the key mediator of the pathogenesis of human neuronal tauopathy in Drosophila . Further, we show that tissue specific downregulation of dMyc ( Drosophila homolog of human c-myc proto-oncogene) alleviates h-tau mediated cellular and functional deficits by restricting the formation of NFTs in neuronal tissues. Therefore, our findings provide very critical and novel insights about pathogenesis of human neuronal tauopathies in Drosophila disease models. [ABSTRACT FROM AUTHOR]

Purpose – Early colonization and balance between the beneficial and pathogenic organisms are essential for good nutrition and health. Ability of probiotic cultures to survive and colonize under the intestinal environmental condition led to their application as functional foods. The paper aims to discuss these issues. Design/methodology/approach – Endeavour has been made to explore the mechanism of gut colonization, selection criteria for probiotic cultures, mechanism of probiotic action, postulated health benefits and prerequisites of a probiotics food. Findings – Probiotic organisms influence the physiological and pathological process of the host by modifying the intestinal microbiota, thereby affecting human health. Postulated health beneficial properties of probiotics suggest their application as functional foods. Originality/value – Ingestion of cultured milk products containing probiotic cultures may provide health benefits in terms of colonization and normalization of intestinal flora and could be recommended for consumption as functional foods. [ABSTRACT FROM AUTHOR]

Purpose – Early colonization and balance between the beneficial and pathogenic organisms are essential for good nutrition and health. Ability of probiotic cultures to survive and colonize under the intestinal environmental condition led to their application as functional foods. The paper aims to discuss these issues. Design/methodology/approach – Endeavour has been made to explore the mechanism of gut colonization, selection criteria for probiotic cultures, mechanism of probiotic action, postulated health benefits and prerequisites of a probiotics food. Findings – Probiotic organisms influence the physiological and pathological process of the host by modifying the intestinal microbiota, thereby affecting human health. Postulated health beneficial properties of probiotics suggest their application as functional foods. Originality/value – Ingestion of cultured milk products containing probiotic cultures may provide health benefits in terms of colonization and normalization of intestinal flora and could be recommended for consumption as functional foods. [ABSTRACT FROM AUTHOR]

Major rice mills of Bangladesh are gradually running out from the paddy processing subsector, a serious concern for national food security. This study investigated the paddy drying methods of 22 rice mills to device a sustainable solution for major rice mills. Weather dependency and high sun drying time (48–96 hours) of paddy are responsible for low capacity utilization of major rice mills. Despite of high demand, appropriate dryer size for major rice mills was still unexplored. Present capacity utilization of major rice mills (27.6%) can be optimized to 72.5% with a 12 ton dryer. Analyzing drying mechanism of recirculating dryers, the study also proposed for a single dryer for both parboiled and aromatic paddy rather than following existing practice. This will make mechanical dryer affordable to major rice mill owners and new investors in this subsector. [ABSTRACT FROM AUTHOR]

Abstract: This study reports on the ion-induced secondary electrons emission (SEE) from MgO films deposited on multiwalled carbon nanotubes (MWCNTs). MWCNTs are grown on quartz substrates using plasma enhanced chemical vapor deposition system and MgO films are deposited on that MWCNTs using electron-beam evaporation technique. The SEE coefficients are obtained from experimentally measured firing voltage. We observed stabilized and lower firing voltage of MgO films deposited on MWCNTs than that for MgO. The experimental results suggest that the density, uniformity and alignment of nanotubes influence the local electric field in nano-pores of MgO films which in turn affects the emission of secondary electrons from MgO surface. [Copyright &y& Elsevier]

The Jaduguda U (-Cu-Fe) deposit in the Singhbhum shear zone has been the most productive uranium deposit in India. Pyrite occurs as disseminated grains or in sulphide stringers and veins in the ore zone. Veins, both concordant and discordant to the pervasive foliation, are mineralogically either simple comprising pyrite ± chalcopyrite or complex comprising pyrite + chalcopyrite + pentlandite + millerite. Nickel-sulphide minerals, though fairly common in concordant veins, are very rare in the discordant veins. Pyrite in Ni-sulphide association is commonly replaced by pentlandite at the grain boundary or along micro-cracks. Based on concentrations of Co and Ni, pyrite is classified as: type-A - high Co (up to 30800 ppm), no/low Ni; type-B - moderate Co (up to 16500 ppm) and moderate to high Ni (up to 32700 ppm); type-C - no/low Co and high Ni (up to 43000 ppm); type-D - neither Co nor Ni. Textural and compositional data of pyrites suggest that the hydrothermal fluid responsible for pre-/early-shearing mineralization evolved from Co-rich to Ni-rich and the late-/post-shearing fluid was largely depleted in minor elements. Sulphur isotope compositions of pyrite mostly furnish positive values ranging between −0.33 and 12.06‰. Composite samples of pyrites with only type-A compositions and mixed samples of type-A and type-B are consistently positive. However, pyrite with mixed type-A and type-C and pyrite with type-D compositions have negative values but close to 0‰. By integrating minor element and sulphur isotope compositions of pyrite in conjunction with other published data on the Jaduguda deposit, it is proposed that reduced sulphur for the precipitation of most pyrites (type-A, type-B) was likely derived from isotopically heavy modified seawater. However, some later sulphur might be magmatic in origin remobilized from existing sulphides in the mafic volcanic rocks in the shear zone. [ABSTRACT FROM AUTHOR]

The design, construction and testing of a rotating energy shifter that simulates the proton energy spectrum of a solar flare event is described. [ABSTRACT FROM PUBLISHER]

Human neurodegenerative polyglutamine [poly(Q)] disorders, such as Huntington's disease (HD) and spinocerebellar ataxias (SCA), are characterised by an abnormal expansion of CAG repeats in the affected gene. The mutated proteins misfold and aggregate to form inclusion bodies that sequester important factors involved in cellular transcription, growth, stress and autophagic response and other essential functions. The insulin signalling pathway has been demonstrated as a major modifier and a potential drug target to ameliorate the poly(Q) mediated neurotoxicity in various model systems. Insulin signalling cascade harbours several downstream sub-pathways, which are synergistically involved in discharging indispensable biological functions such as growth and proliferation, metabolism, autophagy, regulation of cell death pathways etc. Hence, it is difficult to conclude whether the mitigation of poly(Q) neurotoxicity is an accumulative outcome of the insulin cascade, or the result of a specific sub-pathway. For the first time, we report that the ligand binding domain of insulin receptor mediated downstream growth promoting sub-pathway plays the pivotal role in operating the rescue event. We show that the growth promoting activity of insulin cascade is essential to minimize the abundance of inclusion bodies, to restrict neurodegeneration, and to restore the cellular transcriptional balance. Subsequently, we noted the involvement of the mTOR/S6k/4E-BP candidates in mitigating poly(Q) mediated neurotoxicity. Due to the conserved cellular functioning of the insulin cascade across species, and availability of several growth promoting molecules, our results in Drosophila poly(Q) models indicate towards a possibility of designing novel therapeutic strategies to restrict the pathogenesis of devastating human poly(Q) disorders. [Display omitted] • Ligand binding domain of insulin receptor mediates downstream growth promoting branch of insulin signalling in Drosophila. • Growth promoting sub-pathway of insulin signalling is essential to confer rescue against poly(Q) disorders. • Growth promotion is mediated by S6k/4E-BP to restore chromatin architecture and transcriptional balance. • Our study may potentially aid in designing of a novel therapeutic strategy against poly(Q) disorders. [ABSTRACT FROM AUTHOR]

Human tauopathies represent a group of neurodegenerative disorders, characterized by abnormal hyperphosphorylation and aggregation of tau protein, which ultimately cause neurodegeneration. The aberrant tau hyperphosphorylation is mostly attributed to the kinases/phosphatases imbalance, which is majorly contributed by the generation of reactive oxygen species (ROS). Globin(s) represent a well-conserved group of proteins which are involved in O 2 management, regulation of cellular ROS in different cell types. Similarly, Drosophila globin1 (a homologue of human globin) with its known roles in oxygen management and development of nervous system exhibits striking similarities with the mammalian neuroglobin. Several recent evidences support the hypothesis that neuroglobins are associated with Alzheimer's disease pathogenesis. We herein noted that targeted expression of human-tau induces the cellular level of Glob1 protein in Drosophila tauopathy models. Subsequently, RNAi mediated restored level of Glob1 restricts the pathogenic effect of human-tau by minimizing its hyperphosphorylation via GSK-3β/p-Akt and p-JNK pathways. In addition, it also activates the Nrf2-keap1-ARE cascade to stabilize the tau-mediated increased level of ROS. These two parallel cellular events provide a significant rescue against human tau-mediated neurotoxicity in the fly models. For the first time we report a direct involvement of an oxygen sensing globin gene in tau etiology. In view of the fact that human genome encodes for the multiple Globin proteins including a nervous system specific neuroglobin; and therefore, our findings may pave the way to investigate if the conserved oxygen sensing globin gene(s) can be exploited in devising novel therapeutic strategies against tauopathies. [Display omitted] • Human tau (h-tau) driven neurotoxicity induces expression of Glob1 (a Drosophila homologue of human globin). • RNAi mediated restored level of glob1 mitigates h-tau mediated neurotoxicity. • Downregulation of glob1 prevents hyperphosphorylation of tau via GSK-3β/p-Akt and p-JNK pathways. • Downregulation of glob1 activates Nrf2-keap1-ARE cascade to stabilize the level of ROS in h-tau expressing cells. • These two parallel events provide a significant rescue against h-tau mediated neurotoxicity in Drosophila. [ABSTRACT FROM AUTHOR]

Polyglutamine/poly(Q) diseases are a group nine hereditary neurodegenerative disorders caused due to abnormally expanded stretches of CAG trinucleotide in functionally distinct genes. All human poly(Q) diseases are characterized by the formation of microscopically discernable poly(Q) positive aggregates, the inclusion bodies. These toxic inclusion bodies are responsible for the impairment of several cellular pathways such as autophagy, transcription, cell death, etc., that culminate in disease manifestation. Although, these diseases remain largely without treatment, extensive research has generated mounting evidences that various events of poly(Q) pathogenesis can be developed as potential drug targets. The present review article briefly discusses the key events of disease pathogenesis, model system-based investigations that support the development of effective therapeutic interventions against pathogenesis of human poly(Q) disorders, and a comprehensive list of pharmacological and bioactive compounds that have been experimentally shown to alleviate poly(Q)-mediated neurotoxicity. Interestingly, due to the common cause of pathogenesis, all poly(Q) diseases share etiology, thus, findings from one disease can be potentially extrapolated to other poly(Q) diseases as well. [Display omitted] • Polyglutamine/poly(Q) disorders are single gene driven autosomal dominant neurodegenerative diseases. • Abnormal expansion of CAG repeats in the mutated gene codes for a pathogenic protein with an expanded poly(Q) stretch. • Proteins with elongated poly(Q) repeats form neurotoxic aggregates and triggers a cascade of pathogenic events. • Impaired proteostasis, mitochondrial function and cellular transcription are key pathogenic events of poly(Q) disorders. • Such pathogenic events have emerged as potential drug target(s) for further development of novel therapeutics. [ABSTRACT FROM AUTHOR]

• Human tau aggregates migrate trans -cellularly in aging adult Drosophila. • Tau hyperphosphorylation appears to be an important factor for trans -cellular propagation. • Targeted down-regulation of Gsk3β restricts trans -cellular propagation of tau. • This study delivers an easy and rapid in-vivo model for investigation of tau migration pathology. Tauopathies is a class of neurodegenerative disorders which involves the transformation of physiological tau into pathogenic tau. One of the prime causes reported to drive this conversion is tau hyperphosphorylation and the subsequent propagation of pathogenic protein aggregates across the nervous system. Although past attempts have been made to deduce the details of tau propagation, yet not much is known about its mechanism. A better understanding of this aspect of disease pathology can prove to be beneficial for the development of diagnostic and therapeutic approaches. For the first time, we demonstrate that the human tau possesses an intrinsic property to spread trans -cellularly in the fly nervous system irrespective of the tau allele or the neuronal tissue type. Aggregate migration restricted by targeted down-regulation of a specific kinase, elucidates the role of hyper-phosphorylation in its movement. On the contrary to the previous models, our study delivers an easy and rapid in-vivo model for comprehensive examination of tau migration pathology. Henceforth, the developed model would not only be immensely helpful in uncovering the mechanistic in-depths of tau propagation pathology but also aid in modifier and/or drug screening for amelioration of tauopathies. [ABSTRACT FROM AUTHOR]

Functional nanosized two-dimensional clay mineral particles are considered as ideal host materials to manipulate the properties of incorporated organic molecules due to their high cation exchange capacity, layer structure and intercalation properties. The interlayer height of clay layers can be manipulated by simultaneous wetting and drying steps. Here, we have studied the chromatic behaviour of an organic dye generated in-situ from 1,4-di-bis-indolylmethane-benzene in the interlayer space of synthetic saponite (SSA). Initially transparent, self-standing organo-clay hybrid films become red upon heating due to aerobic oxidation suggesting in-situ generation of organic dye and increases the planarity of the intercalated organic molecules. Upon swelling the same hybrid film becomes yellow, due to the partial disturbance in the planarity of generated dye via C-C bond rotation. Simultaneous heating and swelling resulted in a reversible colour transition (clearly visible through the naked eye) between red and yellow for at least 30 cycles. This kind of system may have potential applications as a colorimetric sensor and in the field of optics (optical switching and optical memory etc). Image 1 • Synthesis of tetraindolyl derivative. • Preparation of clay mineral-tetraindolyl hybrid self-standing film. • Colour switching of hybrid film due to the change in gallery height of clay. • Colour switching was reversible with a very good stability. • Such colour switching is suitable for colorimetric sensor, optical switching, optical memory etc. [ABSTRACT FROM AUTHOR]

Visual evidences undeniably appear more convincing since they can be interpreted easily, though may not be always accurate. The electron microscopy techniques not only allow examining the ultra-structure of various cell/tissue types but also help in proposing the in-depth mechanisms of biological processes. Similarly, comprehensive analysis of the neuronal and synaptic communications, and overall integrity of the brain not only helps us to understand its intricate functioning, but also aids in deciphering the complex human brain disorders. The Drosophila brain and the pair of compound eyes have emerged as favoured organs to investigate the fundamentals of nervous system development and disease biology. Various types of electron microscopy techniques have assisted the Drosophila neurobiologists to generate significant insights about the development, structure and function of different neuronal cell types and their contribution in the aetiology of neurodegenerative disorders. The present review provides a snapshot of the applications of various electron microscopy methods in Drosophila neurobiology research. [ABSTRACT FROM AUTHOR]

We theoretically study the properties of thermal conductance in a normal-insulator-superconductor junction of silicene for both thin and thick barrier limit. We show that while thermal conductance displays the conventional exponential dependence on temperature, it manifests a nontrivial oscillatory dependence on the strength of the barrier region. The tunability of the thermal conductance by an external electric field is also investigated. Moreover, we explore the effect of doping concentration on thermal conductance. In the thin barrier limit, the period of oscillations of the thermal conductance as a function of the barrier strength comes out be π/2 when doping concentration in the normal silicene region is small. On the other hand, the period gradually converts to π with the enhancement of the doping concentration. Such change of periodicity of the thermal response with doping can be a possible probe to identify the crossover from specular to retro Andreev reflection in Dirac materials. In the thick barrier limit, thermal conductance exhibits oscillatory behavior as a function of barrier thickness d and barrier height V0 while the period of oscillation becomes V0 dependent. However, amplitude of the oscillations, unlike in tunneling conductance, gradually decays with the increase of barrier thickness for arbitrary height V0 in the highly doped regime. We discuss experimental relevance of our results. [ABSTRACT FROM AUTHOR]

Hemoglobins (Hbs) are evolutionarily conserved small globular proteins with characteristic 3-over-3 α-helical sandwich structure that is typically known as “globin fold”. Hbs have been found to be involved in diverse biological functions and the characteristic property of oxygen transportation is relatively a recent adaptation. Drosophila genome possesses three globin genes ( glob1 , glob2, and glob3 ) and it was previously reported that adequate expression of glob1 is required for various aspects of development, and also to regulate the cellular level of reactive oxygen species (ROS). The present study illustrates the explicit role of glob1 gene in Drosophila development. We demonstrate a dynamic expression pattern of glob1 in larval tissues which largely concentrate around F-actin rich structures and also co-precipitate. Reduced expression of glob1 leads to developmental abnormalities which appeared to be largely mediated by inappropriately formed F-actin based cytoskeletal structures. Our subsequent analysis in FLP/FRT mediated somatic clones establishes specific role of Drosophila glob1 in maintenance of the integrity of F-actin based cytoskeleton during development. For the first time, we report interaction between Glob1 and actin, and propose a novel role of glob1 in maintenance of F-actin based cytoskeleton in Drosophila. [ABSTRACT FROM AUTHOR]

Traumatic brain injuries are highly recognized as one of the leading causes of mortality and morbidity worldwide. A chronic and debilitating condition by nature, TBI is reportedly affecting the socio-economic well-being of society due to the unavailability of effective prophylaxis. Moreover, TBI is responsible for a myriad of systemic complications such as neurological deficits, gastrointestinal dysfunction, visual impairment, and disturbed circadian rhythm, to name a few. With increasing incidences of TBI-associated disabilities, there is an urgent need for better diagnostics and therapeutic interventions. An array of animal models has been developed to recapitulate pathophysiological conditions of TBI and to elucidate the course of cellular and molecular changes. Although mammalian models are pathophysiologically closer to humans, they decelerate the TBI research due to technical limitations. Therefore, various strategies have been established to model TBI in Drosophila that offer several advantages to study various attributes of TBI and provide a great opportunity for large-scale screening of potential drug molecules. In the present review, we have briefly summarized the fundamentals of brain injuries; contemporary advancements, contributions, and scope of Drosophila in TBI research. [Display omitted] • Traumatic brain injury (TBI) is a prominent health hazard affecting majority of population worldwide. • TBI lacks effective preventive measures, diagnostics and therapeutic interventions. • Modeling TBI is higher organisms imposes various technical and ethical limitations. • Drosophila has emerged as a promising organism to model various aspects of TBI for in-depth investigations. [ABSTRACT FROM AUTHOR]

Abstract: Polyglutamine or poly(Q) disorders are dominantly inherited neurodegenerative diseases characterised by progressive loss of neurons in cerebellum, basal ganglia and cortex in adult human brain. Overexpression of human form of mutant SCA3 protein with 78 poly(Q) repeats leads to the formation of inclusion bodies and increases the cellular toxicity in Drosophila eye. The present study was directed to identify a genetic modifier of poly(Q) diseases that could be utilised as a potential drug target. The initial screening process was influenced by the fact of lower prevalence of cancer among patients suffering with poly(Q) disorders which appears to be related to the intrinsic biological factors. We investigated if Drosophila Myc (a homologue of human cMyc proto-oncogene) harbours intrinsic property of suppressing cellular toxicity induced by an abnormally long stretch of poly(Q). We show for the first time that targeted overexpression of Drosophila Myc (dMyc) mitigates the poly(Q) toxicity in eye and nervous systems. Upregulation of dMyc results in a significant reduction in accumulation of inclusion bodies with residual poly(Q) aggregates localising into cytoplasm. We demonstrate that dMyc mediated suppression of poly(Q) toxicity is achieved by alleviating the cellular level of CBP and improved histone acetylation, resulting restoration of transcriptional machinery which are otherwise abbreviated due to poly(Q) disease conditions. Moreover, our study also provides a rational justification of the enigma of poly(Q) patients showing resistance to the predisposition of cancer. [Copyright &y& Elsevier]

Abstract: We report on our study of the influence of varying concentrations of Si doping on the secondary electron emission (SEE) yield of MgO thin films prepared by electron beam evaporation technique. The series of Si-doped MgO films were microstructurally characterized with various tools like X-ray diffraction, scanning electron microscopy and atomic force microscopy. The optimization of the concentration of Si doping is seen to enhance the SEE yield. We discuss the correlation of SEE yield in the context of different deposition and measurement conditions and crystalline orientation. [Copyright &y& Elsevier]

Here, we report the mixing behaviour of diacetylene monomer 10, 12-tricosadiynoic acid (TCDA) and rhodamine-800 (Rh8) using Langmuir–Blodgett (LB) technique. The presence of Rh8 affected the structures, phase behaviour as well as colorimetric properties of TCDA in the mixed films at air–water interface and onto solid support. The mixed LB films having TCDA molefraction ≥ 0.5 leads to multilayer formation, whereas multilayer formation was hardly observed for the films containing TCDA molefraction less than 0.5. It was observed that polymerization as well as phase change (blue to red) was possible only for multilayered films. Brewster angle microscopy, atomic force microscopy, and fluorescence inverted microscopy studies confirmed the formation of definite structures in the polymerized TCDA/Rh8 mixed films at air–water interface and onto solid support. Structure of TCDA polymer strands was largely influenced by the presence of Rh8 in the mixed films. Interestingly, energy transfer occurred from TCDA in red phase to Rh8 in the mixed films with TCDA molefraction greater than 0.4. Maximum energy transfer efficiency was found to be 47.3% for the mixed LB film with TCDA molefraction 0.9. [ABSTRACT FROM AUTHOR]

• Downregulation of dmyc mitigates human-tauV337M mediated neurotoxicity in Drosophila. • Downregulation of dmyc prevents toxic hyperphosphorylation of tauV337M. • Downregulation of dmyc elicits autophagic response in the tau models of Drosophila. Tauopathies such as Alzheimer's disease (AD), Pick's disease (PiD), Frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) etc. represent a group of age-related neurodegenerative disorders in which tau protein loses its normal conformation mostly due to hyperphosphorylation and subsequent formation of the aggregates of defined shapes, known as Neurofibrillary Tangles (NFTs). We have demonstrated earlier that reduced dosage of dmyc (Drosophila homolog of human cmyc proto-oncogene) restricts tauWT mediated disease pathogenesis by regulating the phosphorylation status of tau. We demonstrate further that the downregulation of dmyc also alleviates the mutant human-tau (tauV337M) mediated neurotoxicity in Drosophila by improving disease defects. Moreover, tissue-specific downregulation of dmyc also induces cellular autophagy which facilitates the disposal of misfolded proteins via lysosome-mediated proteostasis. Our findings demonstrate the capability of dmyc in the suppression of different forms of human tauopathies in Drosophila disease models. Interestingly, due to the conserved characteristics of dmyc/cmyc across the animal kingdom, our study strengthens the possibility of utilizing this gene as an effective drug target against tauopathies. [ABSTRACT FROM AUTHOR]

Neurogenesis is driven by spatially and temporally regulated proliferation of neuronal progenitor cells that generates enormous number of assorted neurons to drive the complex behavior of an organism. Drosophila nervous system provides an advantageous model for identification and elucidation of the functional significance of the novel gene(s) involved in neurogenesis. The present study attempts to investigate the role(s) of globin1 (glob1) in the development and maintenance of the nervous system in Drosophila. It is increasingly clear now that globin genes play important role(s) in the various biological phenomena. The vertebrate neuroglobin has been reported to profoundly express in neuronal tissues and provides neuroprotection. We noted ubiquitous presence of Glob1 in the developing neuronal tissues with enhanced concentration throughout the VNC which comprises of midline cell clusters, which subsequently forms numerous types of progenitor cells and finally differentiate into specific neurons of the nervous system. Ubiquitous or pan-neuronal downregulation of glob1 causes partial lethality and mis-positioning of various neural-progenitor cells present in the embryonic midline cell clusters. Subsequently, profound expression of Glob1 was noted in the outer proliferation center of larval brain and photoreceptor axons of optic stalk. The overall arrangement of photoreceptor axons and stereotype positioning of neuroblast cells present in the central region of the brain were severally affected due to reduced expression of glob1. In addition, such larvae and surviving adults develop significant neuro-muscular disabilities. For the first time, our study suggests a novel role of glob1 in development and maintenance of the nervous system adding a new dimension to the functional significance of the multi-tasking glob1 gene in Drosophila. • Glob1 expresses profoundly in VNC during embryogenesis. • OPC and OS of larval brain exhibit enhanced level of Glob1. • Depletion in the expression of glob1 causes mispositioning of various neuronal precursor cells. • Downregulation of glob1 results in neuromuscular disabilities. [ABSTRACT FROM AUTHOR]

Abstract: Plasma enhanced chemical vapor deposition (PECVD) technique using pulsed-DC power supply was used to fabricate diamond like carbon (DLC) films at deposition rates as high as 110 nm/min. The DLC films deposited by pulsed-DC and DC based power supplies under different gas flow ratios were studied for their suitability as dielectric layer coatings in plasma display panels (PDPs). The effect of deposition parameters on the properties of the DLC films were studied using Fourier transform infra-red spectroscopy (FTIR) and spectroscopic ellipsometry (SE). FTIR reveals that higher hydrogen dilution in gas mixture leads to higher sp 3 content. SE studies in wide spectral range were analyzed using Tauc-Lorentz model dielectric function. A rise in the extracted refractive index was seen on increasing the H2 content in the feed gas, thus resulting in optically denser films. Secondary electron emission coefficient (γ) was measured in the films deposited by the DC and pulsed-DC based PECVD. Firing voltage in the DLC samples was found to have very low variation in the operating pressure range used in commercial PDPs, suggesting possibility of enhanced long term reliability of DLC coatings in future PDP applications. [Copyright &y& Elsevier]

The difference in refractive indices of glass substrate and transparent conducting oxide (TCO) electrode causes optical reflection in thin film solar cells, which results in lower absorption of light for devices. An anti-reflection layer between glass and TCO is required to reduce the loss of light due to optical reflection. Silicon nitride (SixNy:Hz) films have shown antireflection property. The refractive index of SixNy:Hz films can be engineered by changing the silicon or nitrogen content in the film. Here, we report the optimization of refractive index of SixNy:Hz to achieve a value between refractive index of glass (1.5) and TCO film (2.0). SixNy:Hz films have been deposited in a RF-plasma enhanced chemical vapour deposition system operating at a frequency of 13.56 MHz. The substrate temperature was fixed at 300 °C. Fourier transform infrared analysis has been used to determine the nature of Si-N, N-H, and Si-H bonding in the films. Refractive index of films has been measured using spectroscopic ellipsometer. The optical reflectance and transmission of SixNy:Hz and SixNy:Hz/TCO layers have been measured using UV/VIS spectrometer. The gas flow rate ratio of N2/SiH4 has been varied from 235 to 470. Decrease in transmittance of SixNy:Hz/TCO layer is observed with increase in silicon concentration in the film. Refractive index of SixNy:Hz also increased with an increase of the silicon content in the films. The reflectance of TCO films has been decreased from 15% to 8% when SixNy:Hz film is incorporated between glass substrate and TCO film. An improvement of around 20% has been observed in current density of solar cells having SixNy:Hz film as refractive index matching layer with refractive index 1.83. Thus, SixNy:Hz film as refractive index matching layer can be used to improve the solar cells device efficiency. [ABSTRACT FROM AUTHOR]