UV-A,B,C Emitting Persistent Luminescent Materials.

The nearly dormant field of persistent luminescence has gained fresh impetus after the discovery of strontium aluminate persistent luminescence phosphor in 1996. Several efforts have been put in to prepare efficient, long decay, persistent luminescent materials which can be used for different applications. The most explored among all are the materials which emit in the visible wavelength region, 400-650 nm, of the electromagnetic spectrum. However, since 2014, the wavelength range is extended further above 650 nm for biological applications due to easily distinguishable signal between luminescent probe and the auto-fluorescence. Recently, UV-emitting persistent materials have gained interest among researchers' due to their possible application in information storage, phototherapy and photocatalysis. In the present review, we summarize these recent developments on the UV-emitting persistent luminescent materials to motivate young minds working in the field of luminescent materials.

Comparison of STONE score, Guy's stone score and Clinical Research Office of the Endourological Society (CROES) score as predictive tools for percutaneous nephrolithotomy outcome: a prospective study.

OBJECTIVE: To evaluate which among the three scoring systems used to predict stone-free status (SFS) after percutaneous nephrolithotomy (PCNL), namely Guy's stone score (GSS), STONE nephrolithometry score and Clinical Research Office of the Endourological Society (CROES) nephrolithometry nomogram, is the most accurate predictor of SFS. METHOD AND MATERIALS: We prospectively included all patients who underwent PCNL (tract size >24 F) at our hospital between July 2017 and January 2019. All demographic and peri-operative data were tabulated including calculation of GSS, STONE score and CROES nomogram score using preoperative computed tomography. Comparison of the 'stone-free' group and 'residual-stone' group was carried out using standard statistical methods. RESULTS: A total of 252 patients were enrolled. The mean GSS, STONE score and CROES score in the stone-free group was 1.60, 6.98 and 212.27, respectively, and in the residual stone group group it was 2.93, 8.98 and 129.89, respectively (P < 0.001 in each). Receiver-operating characteristic (ROC) curves showed that all three scoring systems had similar predictive accuracy for post-PCNL SFS, with STONE score having the highest area under the ROC curve value (0.852). GSS was significantly associated with operating time, estimated blood loss (EBL) and length of hospital stay (LOS; P < 0.001 in each). STONE score and CROES score were both significantly associated with EBL (P = 0.029 and 0.001, respectively). CONCLUSION: All three scoring systems are equally predictive of post-PCNL SFS. EBL is significantly associated with all three scoring systems, while GSS is also associated with operating time and LOS.

A fruit-tissue (apple) based training model for transurethral resection of prostate: face, content and construct validation.

AIMS AND OBJECTIVES: To establish face, content and construct validity of an innovative fruit-tissue (apple) based transurethral resection of prostate (TURP) training model devised at our institute. METHOD AND MATERIAL: Six consultants, three fellows and 16 residents performed TURP on the new fruit-tissue (apple) based TURP model for ten minutes after watching a demo-video. The procedure was videographed. At the end, participants answered a set of questionnaires regarding their experience. The video and the apple both were examined by blinded separate assessors based on pre-decided parameters. Statistical analysis was done to find out the face, content and construct validity of the training model. RESULTS: Participants were divided into two groups, expert and novice, based TURP surgery experience. The model was positively rated (lowest median value 4) by all novice for its 'realism' and 'acceptability'. The expert group also felt that the model reproduced real TURP experience (lowest median value 4). Thus, both face and content validity were established. The expert group resected more tissue (18.3±2.5 gm vs 10.3±3.4 gm; P<0.001) with less irrigation fluid (1566.6±187.0 ml vs 2112.5±344.2 ml; P<0.001) removing more chips (39.8±6.2 vs 25.6±3.0; P<0.001) and orientated themselves faster (63.3±12.2 sec vs 90.3±12.7 sec; P<0.001). The assessors' subjective evaluation of videos and apples both favored the experts. The model can differentiate 'expert' from 'novice', thus establishing 'construct validity'. CONCLUSION: The new fruit-tissue (apple) based TURP model is a realistic and acceptable TRUP training model with proven face, content and construct validity.

Inkjet printing of NiO films and integration as hole transporting layers in polymer solar cells.

Stability concerns of organic solar cell devices have led to the development of alternative hole transporting layers such as NiO which lead to superior device life times over conventional Poly(3,4-ethylenedioxythiophene) Polystyrene sulfonate (PEDOT:PSS) buffered solar cells. From the printability of such devices, it is imperative to be able to print NiO layers in the organic solar cell devices with normal architecture which has so far remained unreported. In this manuscript, we report on the successful ink-jet printing of very thin NiO thin films with controlled thickness and morphology and their integration in organic solar cell devices. The parameters that were found to strongly affect the formation of a thin yet continuous NiO film were substrate surface treatment, drop spacing, and substrate temperature during printing. The effect of these parameters was investigated through detailed morphological characterization using optical and atomic force microscopy and the results suggested that one can achieve a transmittance of ~89% for a ~18 nm thin NiO film with uniform structure and morphology, fabricated using a drop spacing of 50 µm and a heat treatment temperature of 400 °C. The devices fabricated with printed NiO hole transporting layers exhibit power conversion efficiencies comparable to the devices with spin coated NiO films.

Ethosuximide Induces Hippocampal Neurogenesis and Reverses Cognitive Deficits in an Amyloid-ß Toxin-induced Alzheimer Rat Model via the Phosphatidylinositol 3-Kinase (PI3K)/Akt/Wnt/ß-Catenin Pathway.

Neurogenesis involves generation of new neurons through finely tuned multistep processes, such as neural stem cell (NSC) proliferation, migration, differentiation, and integration into existing neuronal circuitry in the dentate gyrus of the hippocampus and subventricular zone. Adult hippocampal neurogenesis is involved in cognitive functions and altered in various neurodegenerative disorders, including Alzheimer disease (AD). Ethosuximide (ETH), an anticonvulsant drug is used for the treatment of epileptic seizures. However, the effects of ETH on adult hippocampal neurogenesis and the underlying cellular and molecular mechanism(s) are yet unexplored. Herein, we studied the effects of ETH on rat multipotent NSC proliferation and neuronal differentiation and adult hippocampal neurogenesis in an amyloid ß (Aß) toxin-induced rat model of AD-like phenotypes. ETH potently induced NSC proliferation and neuronal differentiation in the hippocampus-derived NSC in vitro. ETH enhanced NSC proliferation and neuronal differentiation and reduced Aß toxin-mediated toxicity and neurodegeneration, leading to behavioral recovery in the rat AD model. ETH inhibited Aß-mediated suppression of neurogenic and Akt/Wnt/ß-catenin pathway gene expression in the hippocampus. ETH activated the PI3K·Akt and Wnt·ß-catenin transduction pathways that are known to be involved in the regulation of neurogenesis. Inhibition of the PI3K·Akt and Wnt·ß-catenin pathways effectively blocked the mitogenic and neurogenic effects of ETH. In silico molecular target prediction docking studies suggest that ETH interacts with Akt, Dkk-1, and GSK-3ß. Our findings suggest that ETH stimulates NSC proliferation and differentiation in vitro and adult hippocampal neurogenesis via the PI3K·Akt and Wnt·ß-catenin signaling.

Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways.

The human health hazards related to persisting use of bisphenol-A (BPA) are well documented. BPA-induced neurotoxicity occurs with the generation of oxidative stress, neurodegeneration, and cognitive dysfunctions. However, the cellular and molecular mechanism(s) of the effects of BPA on autophagy and association with oxidative stress and apoptosis are still elusive. We observed that BPA exposure during the early postnatal period enhanced the expression and the levels of autophagy genes/proteins. BPA treatment in the presence of bafilomycin A1 increased the levels of LC3-II and SQSTM1 and also potentiated GFP-LC3 puncta index in GFP-LC3-transfected hippocampal neural stem cell-derived neurons. BPA-induced generation of reactive oxygen species and apoptosis were mitigated by a pharmacological activator of autophagy (rapamycin). Pharmacological (wortmannin and bafilomycin A1) and genetic (beclin siRNA) inhibition of autophagy aggravated BPA neurotoxicity. Activation of autophagy against BPA resulted in intracellular energy sensor AMP kinase (AMPK) activation, increased phosphorylation of raptor and acetyl-CoA carboxylase, and decreased phosphorylation of ULK1 (Ser-757), and silencing of AMPK exacerbated BPA neurotoxicity. Conversely, BPA exposure down-regulated the mammalian target of rapamycin (mTOR) pathway by phosphorylation of raptor as a transient cell's compensatory mechanism to preserve cellular energy pool. Moreover, silencing of mTOR enhanced autophagy, which further alleviated BPA-induced reactive oxygen species generation and apoptosis. BPA-mediated neurotoxicity also resulted in mitochondrial loss, bioenergetic deficits, and increased PARKIN mitochondrial translocation, suggesting enhanced mitophagy. These results suggest implication of autophagy against BPA-mediated neurodegeneration through involvement of AMPK and mTOR pathways. Hence, autophagy, which arbitrates cell survival and demise during stress conditions, requires further assessment to be established as a biomarker of xenoestrogen exposure.

Microscopic Investigations into the Effect of Surface Treatment of Cathode and Electron Transport Layer on the Performance of Inverted Organic Solar Cells.

Surface treatments of various layers in organic solar cells play a vital role in determining device characteristics. In this manuscript, we report on the influence of surface treatment of indium tin oxide (ITO) electrode and electron transport layer (ETL), ZnO, on the photovoltaic performance of inverted organic solar cells (IOSC) and their correlation with the surface chemistry and surface potential as studied using X-ray photoelectron spectroscopy (XPS) and Kelvin probe force microscopy (KPFM), using the device structure glass/ITO/ZnO/P3HT: PCBM/MoO3/(Au or Ag) (P3HT, poly(3-hexylthiophene-2,5-diyl), and PCBM, phenyl-C61-butyric acid methyl ester). Our results show that although ozonization of ITO leads to an improvement in the device power conversion efficiency, the ozonization of a subsequent ZnO layer results in a decreased performance mainly because of a decrease in the fill factor (FF). However, subsequent methanol (CH3OH) treatment of ZnO layer on an ozonized ITO electrode shows substantial improvement with device efficiencies exceeding ∼4% along with superior reproducibility of the devices. Furthermore, a detailed analysis of the surface wettability, chemistry, and surface potential using contact angle measurements, XPS, and KPFM attribute the improvements to the elimination of surface defects and the changes in the surface potential. Finally, impedance analysis suggests that methanol treatment of the ZnO layers leads to the development of a favorable nanophase structure with higher conductivity, which is otherwise indiscernible using microscopic methods.

Curcumin-loaded nanoparticles potently induce adult neurogenesis and reverse cognitive deficits in Alzheimer's disease model via canonical Wnt/ß-catenin pathway.

Neurogenesis, a process of generation of new neurons, is reported to be reduced in several neurodegenerative disorders including Alzheimer's disease (AD). Induction of neurogenesis by targeting endogenous neural stem cells (NSC) could be a promising therapeutic approach to such diseases by influencing the brain self-regenerative capacity. Curcumin, a neuroprotective agent, has poor brain bioavailability. Herein, we report that curcumin-encapsulated PLGA nanoparticles (Cur-PLGA-NPs) potently induce NSC proliferation and neuronal differentiation in vitro and in the hippocampus and subventricular zone of adult rats, as compared to uncoated bulk curcumin. Cur-PLGA-NPs induce neurogenesis by internalization into the hippocampal NSC. Cur-PLGA-NPs significantly increase expression of genes involved in cell proliferation (reelin, nestin, and Pax6) and neuronal differentiation (neurogenin, neuroD1, neuregulin, neuroligin, and Stat3). Curcumin nanoparticles increase neuronal differentiation by activating the Wnt/ß-catenin pathway, involved in regulation of neurogenesis. These nanoparticles caused enhanced nuclear translocation of ß-catenin, decreased GSK-3ß levels, and increased promoter activity of the TCF/LEF and cyclin-D1. Pharmacological and siRNA-mediated genetic inhibition of the Wnt pathway blocked neurogenesis-stimulating effects of curcumin. These nanoparticles reverse learning and memory impairments in an amyloid beta induced rat model of AD-like phenotypes, by inducing neurogenesis. In silico molecular docking studies suggest that curcumin interacts with Wif-1, Dkk, and GSK-3ß. These results suggest that curcumin nanoparticles induce adult neurogenesis through activation of the canonical Wnt/ß-catenin pathway and may offer a therapeutic approach to treating neurodegenerative diseases such as AD, by enhancing a brain self-repair mechanism.

Molecular interaction analysis of cigarette smoke carcinogens NNK and NNAL with enzymes involved in DNA repair pathways: An in silico approach.

DNA damage occurs almost all the times in cells, but is repaired also continuously. Occurrence of all these mutations and their accumulation in one cell which finally becomes tumorigenic/carcinogenic appears possible if the DNA repair mechanism is hampered. We hypothesize that alterations in DNA repair pathways, either all or at least at one i.e. genetic, translational or posttranslational level, becomes quite imperative for the initiation and progression of Cancer. Therefore, we investigated the interaction capability of some carcinogens with the enzymes involved in the DNA repair mechanisms. Cigarette smoke's derivatives like NNK and NNAL are well established carcinogens. Hence, we analyzed 72 enzymes involved in the DNA repair Mechanisms for their interactions with ligands (NNK and NNAL). The binding efficiencies with enzymes ranging from +36.96 to -7.47 Kcal/Mol. Crystal Structure of Human Carbonmonoxy-Haemoglobin at 1.25 Å Resolution, PDB ID-1IRD as a +Ve control, showed binding energy -6.31 to -6.68 Kcal/Mol. and Human heat shock factor-binding protein 1, PDB ID- 3CI9 as a -Ve control, showed - 3.91 to +2.09 Kcal/Mol. Binding was characterized for the enzymes sharing equivalent or better interaction as compared to +Ve control. Study indicated the loss of functions of these enzymes, which probably could be a reason for fettering of DNA repair pathways resulting in damage accumulation and finally cancer formation.