Hydrogen production, storage, and transportation: recent advances.

One such technology is hydrogen-based which utilizes hydrogen to generate energy without emission of greenhouse gases. The advantage of such technology is the fact that the only by-product is water. Efficient storage is crucial for the practical application of hydrogen. There are several techniques to store hydrogen, each with certain advantages and disadvantages. In gaseous hydrogen storage, hydrogen gas is compressed and stored at high pressures, requiring robust and expensive pressure vessels. In liquid hydrogen storage, hydrogen is cooled to extremely low temperatures and stored as a liquid, which is energy-intensive. Researchers are exploring advanced materials for hydrogen storage, including metal hydrides, carbon-based materials, metal-organic frameworks (MOFs), and nanomaterials. These materials aim to enhance storage capacity, kinetics, and safety. The hydrogen economy envisions hydrogen as a clean energy carrier, utilized in various sectors like transportation, industry, and power generation. It can contribute to decarbonizing sectors that are challenging to electrify directly. Hydrogen can play a role in a circular economy by facilitating energy storage, supporting intermittent renewable sources, and enabling the production of synthetic fuels and chemicals. The circular economy concept promotes the recycling and reuse of materials, aligning with sustainable development goals. Hydrogen availability depends on the method of production. While it is abundant in nature, obtaining it in a clean and sustainable manner is crucial. The efficiency of hydrogen production and utilization varies among methods, with electrolysis being a cleaner but less efficient process compared to other conventional methods. Chemisorption and physisorption methods aim to enhance storage capacity and control the release of hydrogen. There are various viable options that are being explored to solve these challenges, with one option being the use of a multilayer film of advanced metals. This work provides an overview of hydrogen economy as a green and sustainable energy system for the foreseeable future, hydrogen production methods, hydrogen storage systems and mechanisms including their advantages and disadvantages, and the promising storage system for the future. In summary, hydrogen holds great promise as a clean energy carrier, and ongoing research and technological advancements are addressing challenges related to production, storage, and utilization, bringing us closer to a sustainable hydrogen economy.

Towards Room Temperature Thermochromic Coatings with controllable NIR-IR modulation for solar heat management & smart windows applications.

Solar heat management & green air-conditioning are among the major technologies that could mitigate heat islands phenomenon while minimizing significantly the CO2 global foot-print within the building & automotive sectors. Chromogenic materials in general, and thermochromic smart coatings especially are promising candidates that consent a noteworthy dynamic solar radiation Infrared (NIR-IR) regulation and hence an efficient solar heat management especially with the expected increase of the global seasonal temperature. Within this contribution, two major challenging bottlenecks in vanadium oxide based smart coatings were addressed. It is validated for the first time that the NIR-IR modulation of the optical transmission (∆TTRANS = T(T〈TMIT) - T(T〉TMIT) of Vanadium oxide based smart coatings can be controlled & tuned. This upmost challenging bottle-neck controllability/tunability is confirmed via a genuine approach alongside to a simultaneous drastic reduction of the phase transition temperature TMIT from 68.8 °C to nearly room temperature. More precisely, a substantial thermochromism in multilayered V2O5/V/V2O5 stacks equivalent to that of standard pure VO2 thin films but with a far lower transition temperature, is reported. Such a multilayered V2O5/V/V2O5 thermochromic system exhibited a net control & tunability of the optical transmission modulation in the NIR-IR (∆TTRANS) via the nano-scaled thickness' control of the intermediate Vanadium layer. In addition, the control of ∆TTRANS is accompanied by a tremendous diminution of the thermochromic transition temperature from the elevated bulk value of 68.8 °C to the range of 27.5-37.5 ºC. The observed remarkable and reversible thermochromism in such multilayered nano-scaled system of V2O5/V/V2O5 is likely to be ascribed to a noteworthy interfacial diffusion, and an indirect doping by alkaline ions diffusing from the borosilicate substrate. It is hoped that the current findings would contribute in advancing thermochromic smart window technology and their applications for solar heat management in glass windows in general, skyscraper especially & in the automotive industry. If so, this would open a path to a sustainable green air-conditioning with zero-energy input.

Thermal conductivity enhancement in gold decorated graphene nanosheets in ethylene glycol based nanofluid.

We report on the synthesis and thermal conductivity of gold nanoparticles (AuNPs) decorated graphene nanosheets (GNs) based nanofluids. The GNs-AuNPs nanocomposites were synthesised using a nanosecond pulsed Nd:YAG laser (wavelength = 1,064 nm) to ablate graphite target followed by Au in ethylene glycol (EG) base fluid to obtain GNs-AuNPs/EG hybrid nanofluid. The characterization of the as-synthesised GNs-AuNPs/EG hybrid nanofluid confirmed a sheet-like structure of GNs decorated with crystalline AuNPs with an average particle diameter of 6.3 nm. Moreover, the AuNPs appear smaller in the presence of GNs which shows the advantage of ablating AuNPs in GNs/EG. The thermal conductivity analysis in the temperature range 25-45 °C showed that GNs-AuNPs/EG hybrid nanofluid exhibits an enhanced thermal conductivity of 0.41 W/mK compared to GNs/EG (0.35 W/mK) and AuNPs/EG (0.39 W/mK) nanofluids, and EG base fluid (0.33 W/mK). GNs-AuNPs/EG hybrid nanofluid displays superior enhancement in thermal conductivity of up to 26% and this is due to the synergistic effect between AuNPs and graphene sheets which have inherent high thermal conductivities. GNs-AgNPs/EG hybrid nanofluid has the potential to impact on enhanced heat transfer technological applications. Also, this work presents a green synthesis method to produce graphene-metal nanocomposites for various applications.

Heterogeneity of histamine H3 receptor genomic expression in the cerebral cortex of spontaneously hypertensive rat.

Specific binding of [3H]-N-alpha-methylhistamine to homogenates from cerebral cortex tissue was analyzed in aged Wistar Kyoto (WKY) and Spontaneously Hypertensive rats (SHR). Scatchard plot analysis of [3H]-N-alpha-methylhistamine binding of the H3 receptor in the cerebral cortex from aged (6, 9, 12, and 16 week) SHR animals indicated that Bmax increased, respectively, 38.05 +/- 1.58, 59.63 +/- 2.48, 79.17 +/- 5.02, and 84.41 +/- 3.72 fmol/mg of protein. Binding studies using tissue from WKY rats indicated that maximal binding (Bmax) of the ligand to the receptor was not significantly altered. The analyses also yielded Kd values of 5, 7.2, 6.3 and 3.8 nM in SHR tissue respectively. Primers based on the sequence of the third intracellular loop of the H3 receptor were amplified at 35 cycles yielding several amplicons. These amplicons expressed sizes 875, 485, and 280 bp in 6 and 9 week cortical tissue from WKY animals where as in cortical tissue from 6 and 9 week SHR animals only two amplicons were expressed, 485 and 280 bp, respectively. Differences in gene expression for 12 and 16 week WKY and SHR rats were also compared using identical primers. Five amplicons were expressed in cortical tissue from 12 and 16 week WKY rats with 1000, 900, 821, 485, and 430 bp where as in 12 and 16 week SHR animals only one amplicon was expressed at 485 bp. The present results imply (1) that H3 receptor density in cortical tissue of SHR animals increases with age where as the number of the expressed amplicons of the detected H3 receptor decreases; and (2) even though a decrease in number of expressed amplicons of the H3 receptor were observed, an increase in expression of the larger amplicon (~500 bp) is evident.

Protein Kinase C- alpha/betaII, delta, and zeta/lambda involvement in ethanol-induced MAPK expression in vascular smooth muscle cells.

Protein Kinase C (PKC) exists as one of twelve serine/threonine isoforms and has been found to mediate ethanol-induced activation of the Mitogen-Activated Protein Kinase (MAPK) pathway. The aim of this study was to determine the PKC isoform(s) that are mediators of ethanol-induced MAPK activity (ERK 1 and 2) and to verify the necessity of calcium in this activation process using cell culture in the presence and absence of ethanol, and other agents that modulate PKC expression. Western blotting analysis was used to assess the effect of ethanol on activating classical (alpha/ssII), novel (delta) and atypical (zeta/lambda) PKC isoforms in vascular smooth muscle cells (VSMCs). The results indicate that ethanol treated VSMCs express the classical PKC-alpha/ssII, novel PKC-delta, and atypical PKC-zeta/lambda isoforms. The expression of PKC-alpha/ssII was inhibited within the first two min of stimulation, followed by activation with maximum expression at 10 min. Similarly, PKC-delta and zeta expressions were suppressed during the first two min of ethanol stimulation with maximum increase in expressions at 10 min. The PKC inhibitor GF109203X and the calcium chelating agent BAPTA, enhanced ethanol-induced PKC expression, whereas, diltiazem reduced expression of PKC by 10% of control. On the other hand, BAPTA in the presence of GF10203X inhibited expression of ERK 1 & 2 downstream from the PKC pathway, whereas, BAPTA alone enhanced expression. These results demonstrate also that classical, novel, and atypical PKCs respond to ethanol during the initial phase of activation of ERK 1 & 2.

Cross-talking between calcium and histamine in the expression of MAPKs in hypertensive vascular smooth muscle cells.

Histamine (HA) is one of many neurotransmitters that have been implicated in cardiovascular functioning. Alterations in vascular smooth muscle due to the effects of histamine have been suggested. We investigated the modulatory effect of HA on mitogen activated protein kinase (MAPK) expression, specifically extracellular regulating kinase (ERK) 1 & 2 in vascular smooth muscle cells (VSMCs) from both spontaneously hypertensive (SHR) and control Wistar Kyoto (WKY) rats. Cross-talking between calcium (Ca2+) and HA during HA-induced modulatory effect on MAPK expression in SHR VSMCs was also investigated. A stimulatory increase in expression of ERK 1 & 2 was observed to be dose and time dependent with maximum expression occurring within 5 min in both SHR and WKY VSMCs. The stimulatory increase in expression is persistent for 60 min in SHR VSMCs, whereas, in WKY cells the stimulatory effect persists for only 20 min. Mepyramine, the H1 receptor antagonist, reduced the HA-induced increase in ERK 1 & 2 significantly in SHR VSMCs. A reduction in the HA stimulated increase in ERK 1 & 2 expression was observed at 20 min of exposing cells to diltiazem, the calcium channel blocker, whereas, the calcium chelator, BAPTA effect on ERK 1 & 2 expression was observed within 5 min in SHR VSMCs. The data demonstrates that cross-talking occurs between HA stimulation and Ca2+ induction during HA-induced activation of ERK 1 & 2 in VSMCs of both cell types. Although both intracellular calcium ([Ca2+]i) and extracellular Ca2+ maybe involved in the activation of ERK 1 & 2 by HA, the dependence on [Ca2+]i is more dramatic than the dependence on extracellular Ca2+ in hypertensive cells, which may contribute to the role of HA as a risk factor of hypertension in VSMCs of the aorta.

Ethanol-induced mitogen activated protein kinase activity mediated through protein kinase C.

The aim of this study was to determine the pathway(s) by which ethanol activates mitogen-activated protein kinase (MAPK) signaling and to determine the role of Ca2+ in the signaling process. MAPK signaling was determined by assessing MAPK activity, measuring phosphorylated extracellular signaling-regulated kinase (pp 44 ERK-1 and pp 42 ERK-2) expression and ERK activity by measuring ERK-2-dependent phosphorylation of a synthetic peptide as a MAPK substrate in rat vascular smooth muscle cells. Ethanol activated extracellular signal-regulated kinase expression (ERK 1 and 2) could be observed when vascular smooth muscle cells (VSMCs) were stimulated for 5 min or less, but was inhibited when cells are treated for 10 min or more with 1-16 mM of ethanol. Maximum ethanol-induced MAPK activity was observed within 5 min with 4 or 8 mM. Ethanol stimulated MAPK activity was blocked by the protein kinase C (PKC) inhibitor (GF109203X) and epidermal growth factor (EGF) receptor antagonist (PD153035) by 41 +/- 24 and 34 +/- 12.3%, respectively. The calcium channel blocker, diltiazem and the chelating agent, BAPTA, reduced the activation of MAPK activity by ethanol, significantly. The data demonstrate that ethanol-stimulated MAPK expression is mediated partially through both the EGF-receptor and PKC intermediates and that activation through the PKC intermediate is calcium-dependent.

Hemicholinium-3 mustard reveals two populations of cycling choline cotransporters in Limulus.

Cholinergic neurons have both a low-affinity and a high-affinity choline transport process. The high-affinity choline transport is sodium dependent and thus it can be referred to as choline cotransport. Choline cotransport has been shown to be up-regulated by neuronal activity. Protein kinase C has also been shown to regulate choline cotransport. Both forms of regulation appear to modulate transport by altering the numbers of choline cotransporters in the nerve terminal membrane. The present study centers on choline cotransporter trafficking in Limulus brain hemi-slice preparations. The competitive, reversible, non-permeant ligand, [3H]hemicholinium-3, was used in binding studies to estimate the relative number of choline cotransporters in plasma membranes. The hemicholinium-3 mustard derivative has been shown to be an irreversible, highly selective, non-permeant ligand for the choline cotransporter, and was also used. Hemicholinium-3 mustard binding to the choline cotransporter blocked [3H]choline transport and [3H]hemicholinium-3 binding. Antecedent elevated potassium exposure of cholinergic tissues has been shown to up-regulate choline transport by the recruitment of additional choline cotransporters to surface membranes. This treatment was also effective in the recruitment of cotransporters following maximal inhibition by hemicholinium-3 mustard of brain hemi-slices. Long-term washout of hemicholinium-3 mustard in hemi-slices resulted in a time-dependent restoration of choline cotransport. Full recovery occurred within 2h. In uninhibited slice preparations, both staurosporine and chelerythrine, protein kinase C inhibitors, stimulated choline uptake. However, within a 1-h washout recovery of uptake following hemicholinium-3 mustard inhibition, the staurosporine responsive but not chelerythrine responsive transport had returned. On the basis of these findings, we hypothesize the existence of two distinct populations of cycling choline cotransporters, which includes inactive or "silent" transporters.

The involvement of protein kinase C in the regulation of choline cotransport in Limulus.

The involvement of protein kinase C (PKC) in the regulation of [3H]choline cotransport was studied in Limulus brain hemi-slice preparations. The PKC activators, phorbol 12-myristate 13-acetate (PMA) or phorbol 12,13-dibutyrate (PDBu), significantly decreased [3H]choline cotransport. Conversely, the PKC inhibitors, staurosporine (STAURO) and polymyxin B (PMB), each increased [3H]choline cotransport. These PKC inhibitors prevented the phorbol ester-induced reduction of transport. Both the PMA induced decrease and the STAURO induced increase in [3H]choline cotransport were paralleled by respective and comparable changes in [3H]hemicholinium-3 (HC-3) specific binding. Pre-exposure of brain hemi-slices to elevated potassium chloride (120 mM KCl) resulted in a doubling of [3H]choline cotransport and [3H]HC-3 binding. The enhancement of [3H]choline cotransport by STAURO and antecedent 120 mM KCl treatment were additive. PMA did not significantly alter elevated potassium stimulated transport. Moreover, arachidonyltrifluoromethyl ketone (AACOCF3) and quinacrine (QUIN), both phospholipase A2 (PLA2) inhibitors, markedly decreased enhanced [3H]choline transport and [3H]HC-3 binding induced by antecedent exposure to depolarizing concentrations of potassium. These results suggest that PKC and PLA2 are involved in the regulation of [3H]choline cotransport but at different regulatory sites.