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P-Type transparent conducting Cu alloyed ZnS thin films from CuZnS targets (, 0.2, 0.3, 0.4, and 0.5) were deposited on glass substrates via radio frequency sputtering. X-ray diffraction and TEM-SAED analysis show that all the films have sphalerite ZnS as the majority crystalline phase. In addition, films with 30% and 40% Cu show the presence of increasing amounts of crystalline Cu2S phase. Conductivity values 400 S were obtained for the films having 30% and 40% Cu, with the maximum conductivity of 752 S obtained for the film with 40% Cu. Temperature dependent electrical transport measurements indicate metallic as well as degenerate hole conductivity in the deposited films. The reflection-corrected transmittance of this Cu alloyed ZnS (40% Cu) film was determined to be 75% at 550 nm. The transparent conductor figure of merit () of the Cu alloyed ZnS (40% Cu), calculated with the average value of transmittance between 1.5 to 2.5 eV, was ≈276 .

Glia is pivotal in regulating neuronal stem cell proliferation, functioning, and nervous system homeostasis, significantly influencing neuronal health and disorders. Dysfunction in glial activity is a key factor in the development and progression of brain pathology. However, a deeper understanding of the intricate nature of glial cells and their diverse role in neurological disorders is still required. To this end, we conducted data mining to retrieve literature from PubMed and Google Scholar using the keywords: glia, Drosophila, neurodegeneration, and mammals. The retrieved literature was manually screened and used to comprehensively understand and present the different glial types in Drosophila, i.e., perineurial, subperineurial, cortex, astrocyte-like and ensheathing glia, their relevance with mammalian counterparts, mainly microglia and astrocytes, and their potential to reveal complex neuron-glial molecular networks in managing neurodegenerative processes., Competing Interests: Declarations Competing interests The authors declare no competing interests. Ethical approval Not applicable., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

We report an organophotoredox-catalyzed silylation/germylation cascade cyclization of N -alkenyl α-CF 3 acrylamides under mild conditions. N -Aminopyridinium salts act as hydrogen atom transfer reagents under photoredox catalysis in the generation of silyl and germyl radicals. An array of silyl- and germyl-substituted 3-CF 3 -4-pyrrolin-2-one derivatives were constructed in a shorter reaction time with low catalyst loading in good to excellent yields at room temperature. Importantly, this protocol is amenable to the late-stage diversification of bioactive molecules, as well as to large-scale synthesis.

Vascular dementia (VaD) is a complex neurodegenerative condition, with cerebral small vessel dysfunctions as the central role in its pathogenesis. Given the lack of suitable animal models to study the disease pathogenesis, we developed a mouse model to closely emulate the clinical scenarios of recurrent transient ischemic attacks (TIAs) leading to VaD using vasoconstricting peptide Endothelin-1(ET-1). We observed that administration of ET-1 led to blood-brain barrier (BBB) disruption and detrimental changes in its components, such as endothelial cells and pericytes, along with neuronal loss and synaptic dysfunction, resulting in irreversible memory loss. Further, in our pursuit of understanding potential interventions, we co-administered pleiotrophin (PTN) alongside ET-1 injections. PTN exhibited remarkable efficacy in preserving vital components of the BBB, including endothelial cells and pericytes, thereby restoring BBB integrity, preventing neuronal loss, and enhancing memory function. Our findings give a valuable framework for understanding the detrimental effects of multiple TIAs on brain health and provide a useful animal model to explore VaD's underlying mechanisms further and pave the way for promising therapies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

We measure the complete set of angular coefficients J_{i} for exclusive B[over ¯]→D^{*}ℓν[over ¯]_{ℓ} decays (ℓ=e, μ). Our analysis uses the full 711  fb^{-1} Belle dataset with hadronic tag-side reconstruction. The results allow us to extract the form factors describing the B[over ¯]→D^{*} transition and the Cabibbo-Kobayashi-Maskawa matrix element |V_{cb}|. Using recent lattice QCD calculations for the hadronic form factors, we find |V_{cb}|=(40.7±0.7)×10^{-3} using the Boyd-Grinstein-Lebed parametrization, compatible with determinations from inclusive semileptonic decays. We search for lepton flavor universality violation as a function of the hadronic recoil parameter w and investigate the differences of the electron and muon angular distributions. We find no deviation from standard model expectations.

Olfml3 is a microglia-specific protein whose role in neuroinflammation is elusive. In silico analysis was conducted to characterize the Olfml3 protein, followed by molecular docking and MD simulation to check possible interaction with Iba1. Further, expression and co-localization analysis was performed in the LPS-induced neuroinflammatory mice brains. Results suggest that Olfml3 physically interacts with Iba1. Olfml3 and Iba1 expression increases during neuroinflammation in mice brains. Olfml3 was observed to co-localize with Iba1, and the number of Olfml3 and Iba1 dual-positive cells increased in the brain of the neuroinflammatory mice model. Thus, Olfml3 could potentially participate in microglia functions by interacting with Iba1., Competing Interests: Declaration of competing interest None., (Copyright © 2024 Elsevier B.V. All rights reserved.)

The ability of metamaterial structures to offer unique properties and new solutions has opened new avenues in a wide range of applications, including super-resolution in optics and efficient antennas in radiofrequency (RF) engineering. In magnetic resonance imaging (MRI), metamaterials hold the promise of increasing the RF magnetic field intensity while minimizing power deposition. Here, we propose a metasurface based on a two-dimensional (2D) array of short conducting strips combined with a high dielectric substrate, which was tuned to operate at ultrahigh field 7T human MRI. While studied in optics and electromagnetics in the GHz-to-THz range, this study is the first to design such a metasurface for proton imaging at 7T MRI. We performed electromagnetic (EM) simulation of the brain MRI setup with the new metasurface placed in the proximity to the temporal lobe, which showed 2.2-fold local increase in the RF transmit efficiency, with superior performance than an array of electric dipoles. In this study, we also investigate the effect of the spatial distribution of the subunits to control the target RF field's distribution. While the common design is based on a uniform distribution of the subunits, nonuniform distribution, such as a denser center (convex) or more condensed edges (concave), provides an extra dimension to tailor both the magnetic and electric fields. The concave distribution achieved 1.5-1.8-fold reduction in the power deposition compared to the uniform distribution in the brain MRI setups examined.

We present the results of a search for the b→dℓ^{+}ℓ^{-} flavor-changing neutral-current rare decays B^{+,0}→(η,ω,π^{+,0},ρ^{+,0})e^{+}e^{-} and B^{+,0}→(η,ω,π^{0},ρ^{+})μ^{+}μ^{-} using a 711  fb^{-1} data sample that contains 772×10^{6}  BB[over ¯] events. The data were collected at the ϒ(4S) resonance with the Belle detector at the KEKB asymmetric-energy e^{+}e^{-} collider. We find no evidence for signal and set upper limits on branching fractions at the 90% confidence level in the range (3.8-47)×10^{-8} depending on the decay channel. The obtained limits are the world's best results. This is the first search for the channels B^{+,0}→(ω,ρ^{+,0})e^{+}e^{-} and B^{+,0}→(ω,ρ^{+})μ^{+}μ^{-}.

Reaction of [V IV O(acac) 2 ] (Hacac = acetylacetone) with a Mannich base, N , N , N ', N '-tetrakis(2-hydroxy-3,5-di- tert- butyl benzyl)-1,2-diaminoethane (H 4 L, I ) in a 1:1 molar ratio in MeOH, leads to the formation of the nonoxidovanadium(IV) complex [V IV L] ( 1 ). Air stable complex 1 has been characterized using various spectroscopic techniques, DFT calculations, and single-crystal X-ray studies. 1 adopts distorted octahedral geometry where ligand coordinates through all coordination functionalities available. This complex has been used as a catalyst in the one-pot, three-component synthesis of 2-amino-3-cyano-4 H -pyrans using 1,3-dicarbonyls (1,3-cyclohexanedione, dimedone, barbituric acid, and 4-hydroxycoumarin), malononitrile, and various substituted aromatic aldehydes in equimolar amounts employing ethanol as a green solvent. The catalytic reaction revealed that the multicomponent synthesis of 4 H -pyrans and chromenes is greatly influenced by both types of 1,3-dicarbonyl compound employed and the nature of the substituent on the aromatic ring of the aldehyde. Synthesized catalyst has also been used in the synthesis of pharmacologically relevant oxygen-containing heterocycles, specifically, 1,8-dioxo-octahydro-1 H -xanthenes and biscoumarins. The possible mechanism for the synthesized one-pot, multicomponent product has been proposed by isolating intermediate(s) generated during synthesis.

We present a comprehensive study of B^{0}→ωω decays using 772×10^{6}  BB[over ¯] pairs collected with the Belle detector at the KEKB e^{+}e^{-} collider. This process is a suppressed charmless decay into two vector mesons and can exhibit interesting polarization and CP violation. The decay is observed for the first time with a significance of 7.9 standard deviations. We measure a branching fraction B=(1.53±0.29±0.17)×10^{-6}, a fraction of longitudinal polarization f_{L}=0.87±0.13±0.13, and a time-integrated CP asymmetry A_{CP}=-0.44±0.43±0.11, where the first uncertainties listed are statistical and the second are systematic. This is the first observation of B^{0}→ωω and the first measurements of f_{L} and A_{CP} for this decay.

We report the results of the first search for B^{-} decays to the Ξ[over ¯]&#95;{c}^{0}Λ[over ¯]&#95;{c}^{-} final state using 711  fb^{-1} of data collected at the ϒ(4S) resonance with the Belle detector at the KEKB asymmetric-energy e^{+}e^{-} collider. The results are interpreted in terms of both direct baryon-number-violating B^{-} decay and Ξ&#95;{c}^{0}-Ξ[over ¯]&#95;{c}^{0} oscillations which follow the standard model decay B^{-}→Ξ&#95;{c}^{0}Λ[over ¯]&#95;{c}^{-}. We observe no evidence for baryon number violation and set the 95% confidence-level upper limits on the ratio of baryon-number-violating and standard model branching fractions B(B^{-}→Ξ[over ¯]&#95;{c}^{0}Λ[over ¯]&#95;{c}^{-})/B(B^{-}→Ξ&#95;{c}^{0}Λ[over ¯]&#95;{c}^{-}) to be <2.7% and on the effective angular frequency of mixing ω in Ξ&#95;{c}^{0}-Ξ[over ¯]&#95;{c}^{0} oscillations to be <0.76  ps^{-1} (equivalent to τ&#95;{mix}>1.3  ps).

Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision.

Brown adipose tissue (BAT) is correlated to cardiovascular health in rodents and humans, but the physiological role of BAT in the initial cardiac remodeling at the onset of stress is unknown. Activation of BAT via 48 h cold (16°C) in mice following transverse aortic constriction (TAC) reduced cardiac gene expression for LCFA uptake and oxidation in male mice and accelerated the onset of cardiac metabolic remodeling, with an early isoform shift of carnitine palmitoyltransferase 1 (CPT1) toward increased CPT1a, reduced entry of long chain fatty acid (LCFA) into oxidative metabolism (0.59 ± 0.02 vs. 0.72 ± 0.02 in RT TAC hearts, p < .05) and increased carbohydrate oxidation with altered glucose transporter content. BAT activation with TAC reduced early hypertrophic expression of β-MHC by 61% versus RT-TAC and reduced pro-fibrotic TGF-β1 and COL3α1 expression. While cardiac natriuretic peptide expression was yet to increase at only 3 days TAC, Nppa and Nppb expression were elevated in Cold TAC versus RT TAC hearts 2.7- and 2.4-fold, respectively. Eliminating BAT thermogenic activation with UCP1 KO mice eliminated differences between Cold TAC and RT TAC hearts, confirming effects of BAT activation rather than autonomous cardiac responses to cold. Female responses to BAT activation were blunted, with limited UCP1 changes with cold, partly due to already activated BAT in females at RT compared to thermoneutrality. These data reveal a previously unknown physiological mechanism of UCP1-dependent BAT activation in attenuating early cardiac hypertrophic and profibrotic signaling and accelerating remodeled metabolic activity in the heart at the onset of cardiac stress., (© 2024 The Author(s). The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.)

The bioavailability of nicotinamide adenine dinucleotide (NAD) is vital for skeletal muscle health, yet the mechanisms or signals regulating NAD homeostasis remain unclear. Here, we uncover a pathway connecting peripheral glucose sensing to the modulation of muscle NAD through TAS1R2, the sugar-sensing G protein-coupled receptor (GPCR) initially identified in taste perception. Muscle TAS1R2 receptor stimulation by glucose and other agonists induces ERK1/2-dependent phosphorylation and activation of poly(ADP-ribose) polymerase1 (PARP1), a major NAD consumer in skeletal muscle. Consequently, muscle-specific deletion of TAS1R2 (mKO) in male mice suppresses PARP1 activity, elevating NAD levels and enhancing mitochondrial capacity and running endurance. Plasma glucose levels negatively correlate with muscle NAD, and TAS1R2 receptor deficiency enhances NAD responses across the glycemic range, implicating TAS1R2 as a peripheral energy surveyor. These findings underscore the role of GPCR signaling in NAD regulation and propose TAS1R2 as a potential therapeutic target for maintaining muscle health., (© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

Motor neuron disorders are diseases that can be passed through generations by heredity or they occur due to spontaneous mutations in the gene. These are the disorders that weaken the connection between motor neurons and the muscles, due to this the coordination between the neurons and muscles gets disturbed and thereby the actions become abnormal, every year millions of people around the world suffer from these different types of motor neuron disorders. Till now there is no proper known treatment for this type of disorder, there is active research work going on to treat these diseases permanently. Some gene therapy treatments are giving promising results in the treatment of these diseases, specifically, genetic modification techniques are the front liners, and many types of nucleases are doing their work to replace the mutated gene with a functional one. Zinc finger nucleases (ZFNs) are one of them with good disease treatment potential with accurate and desirable effects. In this review, we note the complete information about ZFNs and their drawbacks along with their future prospective in gene therapy and also shortly with other types of nucleases-mediated gene therapies. There also some factors that influence the gene therapy treatment are also noted along with some detailed information., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Non-small cell lung carcinoma (NSCLC) exhibits a heightened propensity for brain metastasis, posing a significant clinical challenge. Mucin 5ac (MUC5AC) plays a pivotal role in the development of lung adenocarcinoma (LUAD); however, its role in causing brain metastases remains unknown. In this study, we aimed to investigate the contribution of MUC5AC to brain metastasis in patients with LUAD utilizing various brain metastasis models. Our findings revealed a substantial increase in the MUC5AC level in LUAD brain metastases (LUAD-BrM) samples and brain-tropic cell lines compared to primary samples or parental control cell lines. Intriguingly, depletion of MUC5AC in brain-tropic cells led to significant reductions in intracranial metastasis and tumor growth, and improved survival following intracardiac injection, in contrast to the observations in the control groups. Proteomic analysis revealed that mechanistically, MUC5AC depletion resulted in decreased expression of metastasis-associated molecules. There were increases in epithelial-to-mesenchymal transition, tumor invasiveness, and metastasis phenotypes in tumors with high MUC5AC expression. Furthermore, immunoprecipitation and proteomic analysis revealed a novel interaction of MUC5AC with Annexin A2 (ANXA2), which activated downstream matrix metalloproteases and facilitated extracellular matrix degradation to promote metastasis. Disrupting MUC5AC-ANXA2 signaling with a peptide inhibitor effectively abrogated the metastatic process. Additionally, treatment of tumor cells with an astrocyte-conditioned medium or the chemokine CCL2 resulted in upregulation of MUC5AC expression and enhanced brain colonization. In summary, our study demonstrates that the MUC5AC/ANXA2 signaling axis promotes brain metastasis, suggesting a potential therapeutic paradigm for LUAD patients with high MUC5AC expression., (© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

We measure the tau-to-light-lepton ratio of inclusive B-meson branching fractions R(X&#95;{τ/ℓ})≡B(B→Xτν)/B(B→Xℓν), where ℓ indicates an electron or muon, and thereby test the universality of charged-current weak interactions. We select events that have one fully reconstructed B meson and a charged lepton candidate from 189  fb^{-1} of electron-positron collision data collected with the Belle II detector. We find R(X&#95;{τ/ℓ})=0.228±0.016(stat)±0.036(syst), in agreement with standard-model expectations. This is the first direct measurement of R(X&#95;{τ/ℓ}).

Immune checkpoint inhibition has shown success in treating metastatic cutaneous melanoma but has limited efficacy against metastatic uveal melanoma, a rare variant arising from the immune privileged eye. To better understand this resistance, we comprehensively profile 100 human uveal melanoma metastases using clinicogenomics, transcriptomics, and tumor infiltrating lymphocyte potency assessment. We find that over half of these metastases harbor tumor infiltrating lymphocytes with potent autologous tumor specificity, despite low mutational burden and resistance to prior immunotherapies. However, we observe strikingly low intratumoral T cell receptor clonality within the tumor microenvironment even after prior immunotherapies. To harness these quiescent tumor infiltrating lymphocytes, we develop a transcriptomic biomarker to enable in vivo identification and ex vivo liberation to counter their growth suppression. Finally, we demonstrate that adoptive transfer of these transcriptomically selected tumor infiltrating lymphocytes can promote tumor immunity in patients with metastatic uveal melanoma when other immunotherapies are incapable., (© 2024. The Author(s).)

Metamaterial-based designs in ultra-high field (≥7 T) MRI have the promise of increasing the local magnetic resonance imaging (MRI) signal and potentially even the global efficiency of both the radiofrequency (RF) transmit and receive resonators. A recently proposed metamaterial-like structure-comprised of a high-permittivity dielectric material and a set of evenly distributed copper strips-indeed resulted in a local increase in RF transmission. Here, we demonstrate that non-uniform designs of this metamaterial-like structure can be used to boost the ultimate RF field distribution. A non-uniform dielectric distribution can yield longer electric dipoles, thus extending the RF transmit field coverage. A non-uniform distribution of conducting strips enables the tailoring of the local electric field hot spots, where a concave distribution resulted in lower power deposition. Simulations of the brain and calf regions using our new metamaterial-like design, which combines non-uniform distributions of both the dielectric and conducting strips, revealed a 1.4-fold increase in the RF field coverage compared to the uniform distribution, and a 1.5-2-fold increase in the transmit efficiency compared to the standard surface-coil.

Brain metastasis (BrM) is a major threat to the survival of melanoma, breast, and lung cancer patients. Circulating tumor cells (CTCs) cross the blood-brain barrier (BBB) and sustain in the brain microenvironment. Genetic mutations and epigenetic modifications have been found to be critical in controlling key aspects of cancer metastasis. Metastasizing cells confront inflammation and gradually adapt in the unique brain microenvironment. Currently, it is one of the major areas that has gained momentum. Researchers are interested in the factors that modulate neuroinflammation during BrM. We review here various epigenetic factors and mechanisms modulating neuroinflammation and how this helps CTCs to adapt and survive in the brain microenvironment. Since epigenetic changes could be modulated by targeting enzymes such as histone/DNA methyltransferase, deacetylases, acetyltransferases, and demethylases, we also summarize our current understanding of potential drugs targeting various aspects of epigenetic regulation in BrM., Competing Interests: Conflict of interest statement SKB is a co-founder of Sanguine Diagnostics and Therapeutics, Inc. Other authors declare no competing interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Clinical, epidemiological, and molecular studies have sufficiently highlighted the vitality of vitamin D [25(OH)D and 1,25(OH) 2 D] in human health and wellbeing. Globally, vitamin D deficiency (VDD) has become a public health concern among all age groups. There is a very high prevalence of VDD per the estimates from several epidemiological studies on different ethnic populations. But, population-specific scales do not support these estimates to define VDD clinically and consistent genetic associations. However, clinical studies have shown the relevance of serum vitamin D screening and oral supplementation in improving health conditions, pointing toward a more prominent role of vitamin D in health and wellness. Routinely, the serum concentration of vitamin D is measured to determine the deficiency and is correlated with physiological conditions and clinical symptoms. Recent research points toward a more inclusive role of vitamin D in different disease pathologies and is not just limited to otherwise bone health and overall growth. VDD contributes to the natural history of systemic ailments, including cardiovascular and systemic immune diseases. Considering its significant impact on premature morbidity and mortality, there is a compelling need to comprehensively review and document the direct and indirect implications of VDD in immune system deregulation, systemic inflammatory conditions, and cardio-metabolism. The recommendations from this review call for furthering our research concerning vitamin D and its direct and indirect implications.

Prostate cancer, one of the most frequently diagnosed cancers in men, leads to significant mortality worldwide. Its study is important due to the complexity and diversity in its progression, highlighting the urgent need for improved therapeutic strategies. This chapter probes into the genetic and epigenetic factors influencing prostate cancer progression, underscoring the importance of understanding the disease's molecular fundamentals for the development of targeted therapies. It specifically reviews the role of key genetic mutations in genes such as Androgen Receptor, TP53, SPOP, FOXA1 and PTEN which are crucial for the disease onset and a progression. Furthermore, it examines the impact of epigenetic modifications, including DNA methylation and histone modification, which contribute to the cancer's progression by affecting gene expression and cellular behavior. Further, in this chapter we delve into the underlying signaling mechanism, the advancements in targeting genetic and epigenetic alterations in prostate cancer. These findings have revealed promising targets for therapeutic advancements, aiming to understand and identify promising avenues for future therapies. This chapter improves our current understanding of prostate cancer genetic and epigenetic landscape, emphasizing the necessity of advancing our knowledge to refine and expand treatment options for prostate cancer patients., (Copyright © 2024. Published by Elsevier Inc.)

The N -alkylation of amines with alcohols using earth-abundant and nonprecious metal catalysts has gained considerable attention in the pharmaceutical industry. We described titanium-catalyzed synthetic protocol for N -alkylation of amines with alcohols via borrowing hydrogen or hydrogen autotransfer reactions. The methodology enables the selective monoalkylation of various substituted (hetero)aromatic amines in good to excellent yields (up to 97% yield). The importance of the protocol was further demonstrated by the applicability of earth-abundant metal catalysis and the synthesis of 32 N -alkylated amines. The work allows the utilization of titanium-based catalysts for various reactions to expand the nature blueprint in catalysis.

Aim: We estimated the relationship between routine biochemical laboratory parameters with static bone histomorphometric parameters and their high and low bone turnover capacity predictability in hemodialysis patients., Method: It was a single-center cross-sectional study, included 28 hemodialysis patients. The routine biochemical parameters measured including calcium, phosphorous, alkaline phosphatase, intact PTH, and 25-hydroxycholecalciferol. The histomorphometric parameters assessed were osteoblasts perimeter, osteoclast perimeter, eroded perimeter, osteoid perimeter, bone fibrosis and bone volume., Result: Total 28 hemodialysis patients underwent bone biopsy. Seventy percent were male, with a mean age was 33.07±10.42 yrs; serum alkaline phosphatase was 219.10±311.3IU/ml; vitamin D was 18.18±9.56ng/ml, and intact PTH was 650.7±466.0pg/ml. Intact PTH had a significant positive association with osteoblast, osteoclast, eroded surface, and osteoid perimeter. Serum alkaline phosphatase had a significant relationship with bone fibrosis (r=0.525, p-value=0.004). Intact PTH was significantly higher in females than males (1078.75±533.04 vs. 479.6±309.83; p-value=0.004). The osteoid surface was significantly high in females compared to males (p=0.038). Age had a significant impact on osteoblast and eroded surface (p=0.008 and p=0.031, respectively). Intact PTH is a reliable biomarkers for bone turnover compare to ALP (p<0.001 and p=0.554, respectively)., Conclusion: Intact PTH strongly associated with bone formation, bone resorption parameters. Gender and age had significant impact on static histomorphometric parameters in our study., (Copyright © 2023 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

The conjugation of active biomolecules provides insight into their bioreactivity, leading to many applications in biotechnology and materials science. Herein, we report L-selenocystine (SeC) bioconjugates of lipoic acid (universal antioxidant) and biotin (Vitamin-H). The SeC-bioconjugates, SeC-Biotin (1) and SeC-Lipoic acid (2) were synthesized using solid phase peptide synthesis (SPPS) method and were characterized by multinuclear 1D ( 1 H, 13 C, 77 Se) and 2D ( 1 H- 1 H COSY and 1 H- 13 C TOCSY) NMR spectroscopy, ESI-MS spectrometry, and RP-HPLC. The GPx-like enzyme mimicking activity of the SeC-bioconjugates 1 and 2 has been investigated through the coupled reductase assay method for the catalytic reductions of hydrogen peroxide into water . A significant enhancement in GPx-like enzymatic activity was observed for both novel bioconjugates SeC-Biotin (1) and SeC-Lipoic acid (2) as compared to diphenyl diselenide (Ph 2 Se 2 ), L-selenocystine (SeC), biotin, lipoic acid, and ebselen., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.)

The first simultaneous determination of the absolute value of the Cabibbo-Kobayashi-Maskawa matrix element V&#95;{ub} using inclusive and exclusive decays is performed with the full Belle data set at the ϒ(4S) resonance, corresponding to an integrated luminosity of 711  fb^{-1}. We analyze collision events in which one B meson is fully reconstructed in hadronic modes. This allows for the reconstruction of the hadronic X&#95;{u} system of the semileptonic b→uℓν[over ¯]&#95;{ℓ} decay. We separate exclusive B→πℓν[over ¯]&#95;{ℓ} decays from other inclusive B→X&#95;{u}ℓν[over ¯]&#95;{ℓ} and backgrounds with a two-dimensional fit that utilizes the number of charged pions in the X&#95;{u} system and the four-momentum transfer q^{2} between the B and X&#95;{u} systems. Combining our measurement with information from lattice QCD and QCD calculations of the inclusive partial rate as well as external experimental information on the shape of the B→πℓν[over ¯]&#95;{ℓ} form factor, we determine |V&#95;{ub}^{excl}|=(3.78±0.23±0.16±0.14)×10^{-3} and |V&#95;{ub}^{incl}|=(3.88±0.20±0.31±0.09)×10^{-3}, respectively, with the uncertainties being the statistical error, systematic errors, and theory errors. The ratio of |V&#95;{ub}^{excl}|/|V&#95;{ub}^{incl}|=0.97±0.12 is compatible with unity.

Bakanae disease caused by Fusarium fujikuroi is an emerging disease of rice causing losses in all rice-growing regions around the world. A BC 2 F 2 population was developed by backcrossing the recurrent parent Pusa Basmati 1121 (PB1121) with the recombinant inbred line RIL28, which harbors a major quantitative trait locus (QTL) governing resistance to bakanae, qBK1.2 . MassARRAY-based single-nucleotide polymorphism (SNP) assays targeting the genomic region of qBK1.2 helped in fine mapping the QTL to a region of 130 kb between the SNP markers rs3164311 and rs3295562 using 24 recombinants. In-silico mining of the fine-mapped region identified 11 putative candidate genes with functions related to defense. The expression analysis identified two significantly differentially expressed genes, that is, LOC&#95;Os01g06750 and LOC&#95;Os01g06870 , between the susceptible genotype PB1121 and the resistant genotypes Pusa1342 and R-NIL4. Furthermore, the SNPs identified in LOC&#95;Os01g06750 produced minor substitutions of amino acids with no major effect on the resistance-related functional motifs. However, LOC&#95;Os01g06870 had 21 amino acid substitutions, which led to the creation of the leucine-rich repeat (LRR) domain in the resistant genotype Pusa1342, thereby making it a potential candidate underlying the major bakanae-resistant QTL qBK1.2 . The markers used in the fine mapping program are of immense utility in marker-assisted breeding for bakanae resistance in rice., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2023 Kushwaha, Ellur, Maurya, Krishnan S., Bashyal, Bhowmick, Vinod, Bollinedi, Singh and Singh.)

We present the first comprehensive tests of the universality of the light leptons in the angular distributions of semileptonic B^{0}-meson decays to charged spin-1 charmed mesons. We measure five angular-asymmetry observables as functions of the decay recoil that are sensitive to lepton-universality-violating contributions. We use events where one neutral B is fully reconstructed in ϒ(4S)→BB[over ¯] decays in data corresponding to 189  fb^{-1} integrated luminosity from electron-positron collisions collected with the Belle II detector. We find no significant deviation from the standard model expectations.

Enzalutamide is an androgen receptor (AR) antagonist commonly used in the treatment of prostate cancer (CaP). However, due to the potential toxicity and development of resistance associated with Enzalutamide-based therapy, there is a need to explore additional compounds that can enhance its therapeutic effectiveness while minimizing toxicity. Lupeol is a pharmacologically active triterpene having anticancer effects. The objective of this study was to explore Lupeol's potential in enhancing the chemosensitivity of chemoresistant CaP cells to Enzalutamide in vitro and in a mouse model. To test our hypothesis, we performed cell viability and luciferase reporter gene assay, flow cytometry, animal studies, and histopathological analysis. Finally, we analyzed the change in selective metabolites in the prostate tissue by LCMS. Results demonstrated that a combination of Lupeol and Enzalutamide could better (i) suppress the Cancer Stem Cells (CSCs) and chemoresistant cells (PTEN-CaP8 and PC3) viability and migration, (ii) increase cell cycle arrest, (iii) inhibit the transcriptional activity of AR, c-MYC, c-FLIP, and TCF (iv) inhibit tumor growth in a mouse model (v) protect Enzalutamide-induced adverse effects in prostate glands and gut tissue (vi) decrease levels of testosterone and methionine metabolites. In conclusion, Lupeol enhances the pharmacological efficacy of Enzalutamide and reduces the adverse effects. Thus, Lupeol could be a promising adjuvant for improving Enzalutamide-based treatment outcomes and warrant further research., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2023. Published by Elsevier Inc.)

We measure the lifetime of the D&#95;{s}^{+} meson using a data sample of 207  fb^{-1} collected by the Belle II experiment running at the SuperKEKB asymmetric-energy e^{+}e^{-} collider. The lifetime is determined by fitting the decay-time distribution of a sample of 116×10^{3} D&#95;{s}^{+}→ϕπ^{+} decays. Our result is τ&#95;{D&#95;{s}^{+}}=(499.5±1.7±0.9)  fs, where the first uncertainty is statistical and the second is systematic. This result is significantly more precise than previous measurements.