Pallab Bhattacharya

Graphene decorated with hexagonal shaped M-type ferrite and polyaniline wrapper: a potential candidate for electromagnetic wave absorbing and energy storage device applications

The development of promising microwave absorbing materials is a booming field of research in both the commercial and defense sectors to prevent electromagnetic pollution, and also to enrich the field of stealth technology. Supercapacitors are a symbol of clean energy storage devices. The present work attends to the preparation of hexagonal shaped magnetic M-type hexaferrite, CuFe10Al2O19 (CFA) by a facile chemical co-precipitation method, and the formation of its composites (graphene/CFA) in the presence of acid modified graphene. An in situ approach was employed for the coating of graphene with CFA. Another nanocomposite (graphene/CFA/PANI) was prepared by the wrapping of graphene/CFA with polyaniline (PANI), which was prepared through the in situ chemical oxidation polymerization of aniline. The prepared multifunctional nanocomposites showed an outstanding and improved microwave absorption property (the maximum reflection loss was −63.6 dB at a thickness of 2.5 mm with a broad absorption range) and electrochemical properties (the highest specific capacitance value was 342 F g−1), in contrast to the pristine graphene and CFA. The addition of PANI also improves the microwave absorption and specific capacitance of the nanocomposites. The formation of the multifunctional nanocomposites and their structural characteristics are discussed thoroughly with their impact on the two different fields of applications i.e. microwave absorbing and energy storage device applications individually.

Neuroprotective potential of Piroxicam in cerebral ischemia: An in silico evaluation of the hypothesis to explore its therapeutic efficacy by inhibition of aquaporin-4 and acid sensing ion channel1a

Cerebral stroke is caused by acute interruption of the brain arterial blood supply and is one of the major health problems with no effective treatments so far apart from the thrombolytic recombinant tissue plasminogen activator (rt-PA), which must be administered within 3h of stroke onset. This emerges it as the third leading cause of mortality worldwide. Acidosis and brain edema are the prominent metabolic features of ischemic brain. The combined inhibition of aquaporin-4 (AQP4) and ASIC1a channels may offers a new neuroprotective approach in cerebral stroke management. Moreover, the combined inhibition of AQP4 and ASIC1a with NSAID remains unknown against neuroprotection in animal models of cerebral ischemia. NSAIDs are believed to act as a pharmacological molecule that reported to have an antioxidant and anti-inflammatory properties. Therefore, the target of the present in silico study was to determine the neuroprotective efficacy of Piroxicam, a NSAID in animal model of cerebral ischemia/reperfusion (I/R) injury and efforts were made to analyze its inhibitory effects on aquaporin-4 activation and ASIC1a channels mediated downstream survival/damage mechanisms. Thus we hypothesized that Piroxicam, a NSAID can act as a neuroprotective agent in animal model of cerebral ischemia/reperfusion (I/R) injury due to its inhibitory effects on aquaporin-4 channel and ASIC1a channels. It is indeed vital that we do not give up the fight to develop compounds to treat stroke despite the many years of setbacks. One of the mottos of our proposed hypothesis is to find out a successful modality of effective substantial treatment of brain stroke with other anti stroke therapeutics available till date.

An in-silico strategy to explore neuroprotection by quercetin in cerebral ischemia: A novel hypothesis based on inhibition of matrix metalloproteinase (MMPs) and acid sensing ion channel 1a (ASIC1a)

Cerebral ischemia are caused by acute interruption of the brain arterial blood supply, typically by a thrombus or embolus, leading to neuronal insult and the remainder damage are caused by blood vessel rupture, leading to hemorrhage. Acidosis and matrix metalloproteinase activation are the central and prominent metabolic feature of ischemic brain. The combined inhibition of MMPs and ASIC1a channels can offer a new therapeutic approach in cerebral stroke management. Moreover, the combined inhibition of MMPs and ASIC1a with flavonoids remains unknown against neuroprotection in animal models of cerebral ischemia. Flavonoids are believed to act as health-promoting substances and some of them have antioxidant and anti-inflammatory properties. Therefore, the target of the present study was in-silico evaluation of the neuroprotective efficacy of quercetin in rat model of focal cerebral ischemia/reperfusion (I/R) injury and efforts were made to analyze its inhibitory effects on MMPs activation and ASIC1a channels mediated downstream survival/damage mechanisms. Thus on the basis of our in-silico studies we hypothesize that quercetin can be a neuroprotective agent in rat model of focal cerebral ischemia/reperfusion (I/R) injury due to its inhibitory effects on MMPs activation and ASIC1a channels mediated downstream survival/damage mechanisms.

Polyaniline/HCl/CuCl2/TPU Nanocomposites: Synthesis, Characterization and its Microwave Absorption Behaviour in X-Band

CuCl2-doped polyaniline (PANI)-based microwave absorbing materials were prepared and characterized by different analytical techniques, which confirm the occurance of doping. The electrical conductivity of the nanocomposites was measured by a four-probe method, and the result was explained by considering the complexation between Cu2+ and PANI. Microwave absorption studies were carried out in the X-Band region and discussed with the help of complex permittivity and permeability of the prepared microwave absorbing materials. Microwave absorption result showed that these nanocomposites can be potentially used for various microwave absorbing applications. The thermal stability of the nanocomposites increases due to the incorporation of CuCl2.

Combination therapy of Ifenprodil with Piroxicam may be an effective therapeutic intervention in cerebral stroke: A hypothesis

Owing to the intricate and multifaceted pathology of cerebral stroke, multiple drug therapy had long been suggested for effective stroke treatment. Therefore, the development of a potential new combination of drug is necessitated which can bring about desirable improved neuroprotection targeting different pathways against ischemic stroke. In this context, we hypothesize the combination effect of Piroxicam, a Non steroidal anti inflammatory drug with Ifenprodil, a NR2b selective NMDAR antagonist in animal model of cerebral ischemia. A few past studies have enumerated the neuroprotective roles of Piroxicam and Ifenprodil administered in singlet against cerebral ischemia in animal model, hence we hypothesized that by using Piroxicam and Ifenprodil in combination would provide additive neuroprotection than either of the agents used alone. In this article, we discuss our hypothesis regarding the possibility of Piroxicam and Ifenprodil as a potent combination which may have a positive therapeutic role in treatment of cerebral ischemia through its anti-inflammatory, anti-apoptotic and anti-oxidative characteristics of Piroxicam with Ifenprodil which has been proved to have neuroprotective, anticonvulsant and antinociceptive effects and has potentials for the treatment of several neuropsychiatric disorders, such as Parkinsons disease alcoholism and drug addiction.

Cognitive effects of NSAIDs in cerebral ischemia: a hypothesis exploring mechanical action mediated pharmacotherapy.

Cerebral ischemia is associated with altered neuronal mechanics leading to dynamic reshaping of neuronal structures, giving rise to a cascade of biological pathways leading to many deleterious consequences and cognitive deficits. Memory and learning specifically are mediated by neurotransmitter release from vesicles clustered at the synapse. Mechanical tension is an important factor governing the amount of vesicular neurotransmitter release in response to an action potential. Neuroinflammation in cerebral ischemia leads to altered mechanical/physical forces on neurons which gives rise to abnormal mechanical tension along the neuron resulting in neurotransmitter imbalance leading to cognitive dysfunction. We consider the possibility that modulation of mechanical forces on neurons may be a therapeutic strategy to help prevent cognitive deficit in cerebral ischemia. Here we show how NSAIDs may act as candidate pharmacological molecules which have the ability to inhibit neuroinflammation and which can alter neuronal mechanics by their COX-2 inhibiting property.

Does Piroxicam really protect ischemic neurons and influence neuronal firing in cerebral ischemia? An exploration towards therapeutics.

Cerebral ischemia is still one of the most confusing and enigmatic neurological disorders with least understood injuries. The EEG measures have been traditionally used to detect residual neural dysfunctions after cerebral ischemia although having several shortcomings, yielding controversial and inconsistent results. It is feasible to hypothesize that advanced EEG research can overcome these shortcomings and provide more clear information regarding the long lasting neural impairment in the subjects suffered from brain stroke. To our understanding, EEG power spectrum density measures can significantly contribute towards intervening drug administered diseased model and give us correct status of neuronal firing after an insult. On the basis of our findings we hypothesize that Piroxicam, a non-steroidal anti-inflammatory drug (NSAID) can protect neurons and improves neuronal firing after ischemia/reperfusion injury in animal model of focal cerebral ischemia. This is the first ever finding which advocates the role of Piroxicam, a NSAID in neuronal firing apart from its other neuroprotective roles. Thus, we consider the possibility of modulation of neuronal firing as a therapeutic strategy to help prevent neuronal dysfunctions in cerebral ischemia.

Minocycline and magnesium in combination may be a good therapeutic intervention for cerebral ischemia

A neuroprotective strategy through a combination therapy is always being superior to any other singular therapeutic interventions, as these acts through a multifauceted approach within the brain during cerebral ischemia. Therefore, the development of a potential new combination of drug is necessitated which can bring about desirable improved neuroprotection targeting different pathways against ischemic stroke. Numerous past studies have enumerated the neuroprotective roles of minocycline and magnesium administered in single against cerebral ischemia in animal model hence we hypothesized that by using magnesium with minocycline in combination would provide additive neuroprotection than either of the agents used alone. In this article, we discuss our hypothesis regarding the possibility of minocycline and magnesium as a potent combination which may have a positive therapeutic role in treatment of cerebral ischemia through its anti-inflammatory, anti-apoptotic and anti-oxidative characteristics with magnesium contributing as a regulator of increased calcium influx.