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Traumatic brain injury (TBI) is one of the major health problems worldwide that causes death or permanent disability through primary and secondary damages in the brain. TBI causes primary brain damage and activates glial cells and immune and inflammatory cells, including mast cells in the brain associated with neuroinflammatory responses that cause secondary brain damage. Though the survival rate and the neurological deficiencies have shown significant improvement in many TBI patients with newer therapeutic options, the underlying pathophysiology of TBI-mediated neuroinflammation, neurodegeneration, and cognitive dysfunctions is understudied. In this study, we analyzed mast cells and neuroinflammation in weight drop-induced TBI. We analyzed mast cell activation by toluidine blue staining, serum chemokine C-C motif ligand 2 (CCL2) level by enzyme-linked immunosorbent assay (ELISA), and proteinase-activated receptor-2 (PAR-2), a mast cell and inflammation-associated protein, vascular endothelial growth factor receptor 2 (VEGFR2), and blood-brain barrier tight junction-associated claudin 5 and Zonula occludens-1 (ZO-1) protein expression in the brains of TBI mice. Mast cell activation and its numbers increased in the brains of 24 h and 72 h TBI when compared with sham control brains without TBI. Mouse brains after TBI show increased CCL2, PAR-2, and VEGFR2 expression and derangement of claudin 5 and ZO-1 expression as compared with sham control brains. TBI can cause mast cell activation, neuroinflammation, and derangement of tight junction proteins associated with increased BBB permeability. We suggest that inhibition of mast cell activation can suppress neuroimmune responses and glial cell activation-associated neuroinflammation and neurodegeneration in TBI.

Mast cell activation plays an important role in stress-mediated disease pathogenesis. Chronic stress cause or exacerbate aging and age-dependent neurodegenerative diseases. The severity of inflammatory diseases is worsened by the stress. Mast cell activation-dependent inflammatory mediators augment stress associated pain and neuroinflammation. Stress is the second most common trigger of headache due to mast cell activation. Alzheimer’s disease (AD) is a progressive irreversible neurodegenerative disease that affects more women than men and woman’s increased susceptibility to chronic stress could increase the risk for AD. Modern life-related stress, social stress, isolation stress, restraint stress, early life stress are associated with an increased level of neurotoxic beta amyloid (Aβ) peptide. Stress increases cognitive dysfunction, generates amyloid precursor protein (APP), hyperphosphorylated tau, neurofibrillary tangles (NFTs), and amyloid plaques (APs) in the brain. Stress-induced Aβ persists for years and generates APs even several years after the stress exposure. Stress activates hypothalamic-pituitary adrenal (HPA) axis and releases corticotropin-releasing hormone (CRH) from hypothalamus and in peripheral system, which increases the formation of Aβ, tau hyperphosphorylation, and blood-brain barrier (BBB) disruption in the brain. Mast cells are implicated in nociception and pain. Mast cells are the source and target of CRH and other neuropeptides that mediate neuroinflammation. Microglia express receptor for CRH that mediate neurodegeneration in AD. However, the exact mechanisms of how stress-mediated mast cell activation contribute to the pathogenesis of AD remains elusive. This mini-review highlights the possible role of stress and mast cell activation in neuroinflammation, BBB, and tight junction disruption and AD pathogenesis.

Mast cells are localized throughout the body and mediate allergic, immune, and inflammatory reactions. They are heterogeneous, tissue-resident, long-lived, and granulated cells. Mast cells increase their numbers in specific site in the body by proliferation, increased recruitment, increased survival, and increased rate of maturation from its progenitors. Mast cells are implicated in brain injuries, neuropsychiatric disorders, stress, neuroinflammation, and neurodegeneration. Brain mast cells are the first responders before microglia in the brain injuries since mast cells can release prestored mediators. Mast cells also can detect amyloid plaque formation during Alzheimer's disease (AD) pathogenesis. Stress conditions activate mast cells to release prestored and newly synthesized inflammatory mediators and induce increased blood-brain barrier permeability, recruitment of immune and inflammatory cells into the brain and neuroinflammation. Stress induces the release of corticotropin-releasing hormone (CRH) from paraventricular nucleus of hypothalamus and mast cells. CRH activates glial cells and mast cells through CRH receptors and releases neuroinflammatory mediators. Stress also increases proinflammatory mediator release in the peripheral systems that can induce and augment neuroinflammation. Post-traumatic stress disorder (PTSD) is a traumatic-chronic stress related mental dysfunction. Currently there is no specific therapy to treat PTSD since its disease mechanisms are not yet clearly understood. Moreover, recent reports indicate that PTSD could induce and augment neuroinflammation and neurodegeneration in the pathogenesis of neurodegenerative diseases. Mast cells play a crucial role in the peripheral inflammation as well as in neuroinflammation due to brain injuries, stress, depression, and PTSD. Therefore, mast cells activation in brain injury, stress, and PTSD may accelerate the pathogenesis of neuroinflammatory and neurodegenerative diseases including AD. This review focusses on how mast cells in brain injuries, stress, and PTSD may promote the pathogenesis of AD. We suggest that inhibition of mast cells activation and brain cells associated inflammatory pathways in the brain injuries, stress, and PTSD can be explored as a new therapeutic target to delay or prevent the pathogenesis and severity of AD.

Neuroinflammatory response is primarily a protective mechanism in the brain. However, excessive and chronic inflammatory responses can lead to deleterious effects involving immune cells, brain cells and signaling molecules. Neuroinflammation induces and accelerates pathogenesis of Parkinson’s disease (PD), Alzheimer’s disease (AD) and Multiple sclerosis (MS). Neuroinflammatory pathways are indicated as novel therapeutic targets for these diseases. Mast cells are immune cells of hematopoietic origin that regulate inflammation and upon activation release many proinflammatory mediators in systemic and central nervous system (CNS) inflammatory conditions. In addition, inflammatory mediators released from activated glial cells induce neurodegeneration in the brain. Systemic inflammation-derived proinflammatory cytokines/chemokines and other factors cause a breach in the blood brain-barrier (BBB) thereby allowing for the entry of immune/inflammatory cells including mast cell progenitors, mast cells and proinflammatory cytokines and chemokines into the brain. These peripheral-derived factors and intrinsically generated cytokines/chemokines, α-synuclein, corticotropin-releasing hormone (CRH), substance P (SP), beta amyloid 1–42 (Aβ1–42) peptide and amyloid precursor proteins can activate glial cells, T-cells and mast cells in the brain can induce additional release of inflammatory and neurotoxic molecules contributing to chronic neuroinflammation and neuronal death. The glia maturation factor (GMF), a proinflammatory protein discovered in our laboratory released from glia, activates mast cells to release inflammatory cytokines and chemokines. Chronic increase in the proinflammatory mediators induces neurotoxic Aβ and plaque formation in AD brains and neurodegeneration in PD brains. Glial cells, mast cells and T-cells can reactivate each other in neuroinflammatory conditions in the brain and augment neuroinflammation. Further, inflammatory mediators from the brain can also enter into the peripheral system through defective BBB, recruit immune cells into the brain, and exacerbate neuroinflammation. We suggest that mast cell-associated inflammatory mediators from systemic inflammation and brain could augment neuroinflammation and neurodegeneration in the brain. This review article addresses the role of some atypical inflammatory mediators that are associated with mast cell inflammation and their activation of glial cells to induce neurodegeneration.

Alzheimer’s disease (AD) is characterized by the presence of neuropathological lesions containing amyloid plaques (APs) and neurofibrillary tangles (NFTs). AD is associated with mitochondrial dysfunctions, neuroinflammation and neurodegeneration in the brain. We have previously demonstrated enhanced expression of the proinflammatory protein glia maturation factor (GMF) in glial cells near APs and NFTs in the AD brains. Parahippocampal gyrus consisting of entorhinal and perirhinal subdivisions of temporal cortex is the first brain region affected during AD pathogenesis. Current paradigm implicates oxidative stress-mediated neuronal damage contributing to the early pathology in AD with mitochondrial membrane potential regulating reactive oxygen species (ROS) production. The inner mitochondrial membrane anion transporters called the uncoupling proteins (UCPs), function as regulators of cellular homeostasis by mitigating oxidative stress. In the present study, we have analyzed the expression of GMF and mitochondrial UCP2 and UCP4 in the parahippocampal gyrus of AD and non-AD brains by immunostaining techniques. APs were detected by thioflavin-S fluorescence staining or immunohistochemistry (IHC) with 6E10 antibody. Our current results suggest that upregulation of GMF expression is associated with down-regulation of UCP2 as well as UCP4 in the parahippocampal gyrus of AD brains as compared to non-AD brains. Further, GMF expression is associated with up-regulation of inducible nitric oxide synthase (iNOS), the enzyme that induces the production of nitric oxide (NO), as well as nuclear factor kB p65 (NF-κB p65) expression. Also, GMF appeared to localize to the mitochondria in AD brains. Based on our current observations, we propose that enhanced expression of GMF down-regulates mitochondrial UCP2 and UCP4 thereby exacerbating AD pathophysiology and this effect is potentially mediated by iNOS and NF-κB. Thus, GMF functions as an activator protein that interferes with the cytoprotective mechanisms in AD brains.

Parkinson's disease (PD) is characterized by the presence of Lewy bodies and degeneration of dopaminergic neurons. 1-methyl-4-phenylpyridinium (MPP+), a metabolite of neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and Lewy body component α-synuclein activates glia in PD pathogenesis. Mast cells and glia maturation factor (GMF) are implicated in neuroinflammatory conditions including Multiple Sclerosis. However, the role of mast cells in PD is not yet known. We have analyzed the effect of recombinant GMF, MPP+, α-synuclein and interleukin-33 (IL-33) on mouse bone marrow-derived cultured mast cells (BMMCs), human umbilical cord blood-derived cultured mast cells (hCBMCs) and mouse brain-derived cultured astrocytes by quantifying cytokines/chemokines released using ELISA or by detecting the expression of co-stimulatory molecules CD40 and CD40L by flow cytometry. GMF significantly released chemokine (C-C motif) ligand 2 (CCL2) from BMMCs but its release was reduced in BMMCs from GMF knockout mice. GMF, α-synuclein and MPP+ released IL-1β, β-hexosaminidase from BMMCs, and IL-8 from hCBMCs. GMF released CCL5, and IL-33- induced the expression of GMF from hCBMCs. Novel GMF expression was detected in hCBMCs and BMMCs by immunocytochemistry. GMF released tumor necrosis factor-alpha (TNF-α) from mouse astrocytes, and this release was greater in BMMC- astrocyte coculture than in individual cultures. Flow cytometry results showed increased IL-33 expression by GMF and MPP+, and GMF-induced CD40 expression in astrocytes. Proinflammatory mediator release by GMF, MPP+ and α-synuclein, as well as GMF expression by mast cells indicate a potential therapeutic target for neurodegenerative diseases including PD.

Cobalt phosphides have been investigated as potentially useful electrocatalysts for accelerating hydrogen evolution. Cobalt phosphide electrocatalysts are synthesized in a single step at varied phosphating temperatures (350, 400, 450 °C) via the gas phase approach. Synthesized at a phosphating temperature of 350 °C, Co2P (CP‐350) transforms into a mixed phase that contains both Co2P and CoP (CP‐400 and CP‐450) as the phosphating temperature goes up which is confirmed by XRD. CP‐350, CP‐400, and CP‐450 exhibited overpotentials of 181, 270, and 293 mV respectively with Tafel slopes of 112, 146, and 175 mV/dec. In contrast to CP‐400 and CP‐450, CP‐350 revealed superior hydrogen evolution reaction (HER) performance and stability for up to 12 h due to its pure phase (Co2P), high surface area (151 m2/g), and high electrochemical surface area (7.02 cm2) with low charge transfer resistance. According to our work, changing the phase and active surface area of transition metal phosphide catalysts can greatly increase their HER catalytic efficiency. [ABSTRACT FROM AUTHOR]

Abstract Crop production is impacted by increased plant diseases and shifting environmental circumstances. Monitoring plant health is necessary to raise crop quality and productivity to meet population growth demands. Nanotechnology‐based sensor platforms provide real‐time plant monitoring capabilities, going beyond the constraints of conventional sensor technologies. Wearables are an evolving area of health monitoring and have been modified for agricultural purposes. Wearable sensors are placed on various plant organs in the agricultural industry to check the crops’ health continuously. The varieties of wearable sensor materials and their fabrications, followed by their sensing mechanisms, are highlighted in this review. Furthermore, monitoring plant micro‐environmental factors, including salinity, hazardous gases, and pesticides, are discussed. This text covers various internal plant growth factors monitoring, such as sap flow, transpiration, and signal monitoring. The challenges of wearable sensors in agriculture are mentioned toward the end.

Abstract  The perirhinal cortex (area 35) is well-known locus for neurofibrillary tangles (NFT) in initial Alzheimer’s disease (AD) and fully developed AD and may contain tau alterations in non-demented elderly. The topography and location of this vulnerable cortex, however, is difficult to appreciate because of its variable architecture and to deviations imposed by temporal sulcal patterns. We have immunostained human brains with a short duration of dementia using antibody AT8, which recognize abnormally hyperphosphorylated tau, calcium binding protein-parvalbumin and other phenotype markers to more fully appreciate the extent of area 35 before it is obscured by pathology. We have observed in the mildly affected AD tau immunoreactive lesion that extends from the temporopolar/insular region anteriorly to the posterior parahippocampal cortex. In its anterior–posterior course, it covers the medial bank of the collateral sulcus. Although the tau lesion encroaches slightly into the temporopolar cortex (area TG) anteriorly and medially and the ectorhinal cortex (area 36) laterally, area 35 is unambiguously defined. Ventromedial temporal pathology as revealed by AT8 suggests the presence of a relatively large lesion early in AD involving all of the perirhinal cortex and other non-isocortical areas. The present study demonstrated that the early stage AD patients exhibited AT8 immunoreactive cells in the temporopolar, hippocampus, perirhinal, entorhinal, and insular cortices. [ABSTRACT FROM AUTHOR]

Abstract Tailoring the surface properties by varying the chemistry and roughness could be of interest for self-cleaning applications. We demonstrate the transformation of hydrophobic ZnO Nano rod (NR) array into superhydrophobic nature by changing the local chemical state and without altering the surface roughness by swift heavy ion (SHI) irradiation. The aligned ZnO NR arrays were irradiated using 150 MeV Ag ions with different fluences from 5E10 to 3E12 ions/cm2. The observed static water contact angles of ZnO NRs samples were 103° ± 3°, 152° ± 4°,161° ± 3°, 164° ± 2°, 167° ± 2°,154 ± 3° and 151° ± 2° for the pristine, ion fluencies of 1E11, 3E11, 5E11, 7E11, 1E12 and 3E12 ions cm−2, respectively. The change in local surface chemistry via formation of surface oxygen related defects due to electronic excitations induced by ion irradiation determine the water dewetting properties. It is found that surface oxygen related defects could be tuned by varying the fluence of the SHIs. Durability tests show that the SHI induced surface oxygen-deficient ZnO NRs have the stable superhydrophobic behavior for more than a year.

The study was aimed to validate and optimize high performance thin layer chromatography (HPTLC) method for the determination of phenolic compound hydroxycinnamic acid derivatives from the fruits of Solanum lycopersicum (tomato). The presence of caffeic acid and coumaric acid in the aqueous extracts of S. lycopersicum was observed in spectrophotometer at 200-400 nm. The phenolic functional group was recorded by FTIR analysis. In the HPTLC analysis, the pre-coated silica gel was used as the stationary phase. The solvent mixture containing toluene:ethyl acetate:formic acid:methanol (3:6:1.6:0.4) was identified as an optimum ratio were used as a mobile phase. The chromatograms of the extract was scanned by densitometer at 327 nm. The Rf values (0.67 and 0.69) and finger print data were recorded by WIN CATS software. The developed HPTLC methods for bioactive marker compounds present in the fruit were found to be simple, accurate, and economical.

AbstractWe report the growth and characterization of Fe-Ga thin films. These films were RF sputtered onto Si, MgO and quartz substrates by controlling the parameters such as the deposition time, power and substrate temperature. The deposited films were characterized using X-Ray Diffraction, Atomic Force Microscopy and Vibration Sample Magnetometry measurements. The effect of substrates on the structure and magnetic properties were studied. XRD pattern of the deposited films showed the formation of DO3 phase with L12 ordered structure at higher sputtering power. The room temperature deposited films demonstrated higher magnetization (0.08 emu/g) as compared to higher substrate temperature (300 °C) deposited films. The Mr/Ms ratio was found to be 0.037 for films deposited at room temperature and 0.009 for the substrate temperature 300 °C. L12 order was observed in films deposited on MgO and Quartz substrates. Magnetization was also found to be high (Ms out of plane = 518 emu/cm3, Ms in plane = 707 emu/cm3) for films deposited on MgO substrate.

We demonstrate the multi-functionality engineering on nanocomposite by combining one dimensional (1D) ZnO nanorod (NR) and two dimensional (2D) reduced graphene oxide (rGO) for efficient water remediation. Nano-engineered ZnO NR-rGO nanocomposites show efficient water remediation in terms of degradation of organic dyes and removal of heavy metal ions. Herein, we report on the fabrication of ZnO NR-rGO nanocomposite via a facile template-free hydrothermal route with an aim to improve the visible photocatalytic efficiency of the ZnO NR based nanocomposites. The structural and morphological features reveal that the rGO sheets are attached on the ZnO NRs and form a hybrid composite assembly. The surface enabled ZnO NR-rGO nanocomposites were used to degrade organic dye molecules (methylene blue (MB), methyl orange (MO) and rhodamine B (RhB)) under visible irradiation and adsorb Cu (II) and Co (II) ions from water through an adsorption process. The nanocomposite containing 7.5 wt% rGO and ZnO NRs shows a 4-fold enhancement in the visible photocatalytic activity and effective removal of Cu (II) and Co (II) ions from aqueous solution respectively. The photocatalytic performance is discussed in detail with respect to interaction between ZnO NRs and rGO sheets, light-harvesting properties of the nanocomposites. The effective experimental adsorption data also fit very well with the pseudo-second-order model which reveals the surface adsorption of metal ions. The results provide insight into a new method utilize for both visible photo degradation and adsorption for the removal of various wastewater pollutants. Construction of hybrid form of nanostructures delivers the effective catalytic properties with tunable functionalities for the water remediation. [ABSTRACT FROM AUTHOR]