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This article is devoted to the synthesis of a new magnetic palladium catalyst that has been immobilized on A-TT-Pd coated-magnetic Fe 3 O 4 nanoparticles. Such surface functionalization of magnetic particles is a promising method to bridge the gap between heterogeneous and homogeneous catalysis approaches. The structure, morphology, and physicochemical properties of the particles were characterized through different analytical techniques, including TEM, FT-IR, XRD, SEM, EDS, TGA-DTG, ICP, and VSM techniques. The obtained Fe 3 O 4 @SiO 2 @A-TT-Pd performance can show excellent catalytic activity for the synthesis of diaryl ethers and oxidation of sulfides, and the corresponding products were obtained with high yields. The advantages of this catalyst include a simple test method, green reaction conditions, no use of dangerous solvents, short reaction time, low catalyst loading, and reusability. Also, the nanocatalyst was easily separated from the reaction mixture with the help of a bar magnet and recovered and reused several times without loss of stability and activity.

In this study, the AlFe 2 O 4 @n-Pr@Et-SO 3 H heterogeneous catalyst was successfully synthesized and utilized to produce biodiesel from oleic acid through an esterification process and to oxidize sulfides. To examine the physicochemical characteristics of the AlFe 2 O 4 @n-Pr@Et-SO 3 H nanomaterial, a variety of advanced techniques were employed, including Fourier Transform infrared spectroscopy (FT-IR), Field emission scanning electron microscopy (FE-SEM), Energy dispersive X-ray spectroscopy (EDX), Vibrating sample magnetometer (VSM), Elemental Mapping, Transmission electron microscopy (TEM), Inductively coupled plasma (ICP), and X-ray diffraction (XRD). The AlFe 2 O 4 @n-Pr@Et-SO 3 H materials demonstrated excellent performance in both the esterification of oleic acid and the oxidation of sulfides. Moreover, the catalyst can be easily recovered and reused multiple times without a significant reduction in its effectiveness.

Exposure to genotoxic agents, such as irradiation produces DNA damage, the toxicity of which is augmented when the DNA repair is impaired. Poly (ADP-ribose) polymerase (PARP) inhibitors were found to be \"synthetic lethal\" in cells deficient in BRCA1 and BRCA2 that impair homologous recombination. However, since many tumors, including prostate cancer (PCa) rarely have on such mutations, there is considerable interest in finding alternative determinants of PARP inhibitor sensitivity. We evaluated the effectiveness of radiation in combination with the PARP inhibitor, rucaparib in PCa cells. The combination index for clonogenic survival following radiation and rucaparib treatments revealed synergistic interactions in a panel of PCa cell lines, being strongest for LNCaP and VCaP cells that express ETS gene fusion proteins. These findings correlated with synergistic interactions for senescence activation, as indicated by β--galactosidase staining. Absence of PTEN and presence of ETS gene fusion thus facilitated activation of senescence, which contributed to decreased clonogenic survival. Increased radiosensitivity in the presence of rucaparib was associated with persistent DNA breaks, as determined by χ-H2AX, p53BP1, and Rad51 foci. VCaP cells, which harbor the TMPRSS2-ERG gene fusion and PC3 cells that stably express a similar construct (fusion III) showed enhanced sensitivity towards rucaparib, which, in turn, increased the radiation response to a similar extent as the DNA-PKcs inhibitor NU7441. Rucaparib radiosensitized PCa cells, with a clear benefit of low dose-rate radiation (LDR) administered over a longer period of time that caused enhanced DNA damage. LDR mimicking brachytherapy, which is used successfully in the clinic, was most effective when combined with rucaparib by inducing persistent DNA damage and senescence, leading to decreased clonogenic survival. This combination was most effective in the presence of the TMPRSS2-ERG and in the absence of PTEN, indicating clinical potential for brachytherapy in patients with intermediate and high risk PCa.

Tamil Nadu’s coastal districts frequently experience flooding, with Tuticorin being especially susceptible because of its low-lying terrain, estuarine systems, and concentration of industrial and subsistence activities. This study defines flood hazard zones in Tuticorin district using a multi-criteria decision-making framework based on the Analytic Hierarchy Process (AHP) and a GIS. Important variables were weighted using AHP and included in a GIS environment. These factors included rainfall, drainage density, slope, land use/cover, distance from a river, and flow length. About 85% of the district is located in high to very high flood hazard zones, primarily in coastal villages, salt pan areas, and urban communities close to estuaries. The remaining 0.47% of the district is categorised as low hazard. The results point to important hotspots that need focused interventions for infrastructure development, land-use planning, and catastrophe risk reduction. The method provides a repeatable decision-support tool for climate-resilient planning and shows how GIS-AHP Flood Hazard Zonation may be used for additional susceptible coastal districts in India outside of Tuticorin.

Zika virus (ZIKV) and dengue virus (DENV) are members of the Flaviviridae family of RNA viruses and cause severe disease in humans. ZIKV and DENV share over 90% of their genome sequences, however, the clinical features of Zika and dengue infections are very different reflecting tropism and cellular effects. Here, we used simultaneous RNA sequencing and ribosome footprinting to define the transcriptional and translational dynamics of ZIKV and DENV infection in human neuronal progenitor cells (hNPCs). The gene expression data showed induction of aminoacyl tRNA synthetases (ARS) and the translation activating PIM1 kinase, indicating an increase in RNA translation capacity. The data also reveal activation of different cell stress responses, with ZIKV triggering a BACH1/2 redox program, and DENV activating the ATF/CHOP endoplasmic reticulum (ER) stress program. The RNA translation data highlight activation of polyamine metabolism through changes in key enzymes and their regulators. This pathway is needed for eIF5A hypusination and has been implicated in viral translation and replication. Concerning the viral RNA genomes, ribosome occupancy readily identified highly translated open reading frames and a novel upstream ORF (uORF) in the DENV genome. Together, our data highlight both the cellular stress response and the activation of RNA translation and polyamine metabolism during DENV and ZIKV infection.

How tumour suppressor p53 bifurcates cell cycle arrest and apoptosis and executes these distinct pathways is not clearly understood. We show that BAX and PUMA promoters harbour an identical MAR element and are transcriptional targets of SMAR1. On mild DNA damage, SMAR1 selectively represses BAX and PUMA through binding to the MAR independently of inducing p53 deacetylation through HDAC1. This generates an anti‐apoptotic response leading to cell cycle arrest. Importantly, knockdown of SMAR1 induces apoptosis, which is abrogated in the absence of p53. Conversely, apoptotic DNA damage results in increased size and number of promyelocytic leukaemia (PML) nuclear bodies with consequent sequestration of SMAR1. This facilitates p53 acetylation and restricts SMAR1 binding to BAX and PUMA MAR leading to apoptosis. Thus, our study establishes MAR as a damage responsive cis element and SMAR1–PML crosstalk as a switch that modulates the decision between cell cycle arrest and apoptosis in response to DNA damage.

Environmental anxieties such as high salinity, drought and extreme temperatures are major abiotic stresses that influence plant survival, growth, productivity and geographical distribution of many essential significant crops over the globe. Plants react to these environmental cues by means of cellular, physio-biochemical and molecular processes, results in adjustment of metabolic and structural alterations and adaptation in plants largely controlled by cascades of molecular networks/ pathways. In recent past dehydration-responsive element-binding (DREB) proteins have been extensively studied and contemplated in improving tolerance to abiotic stresses. This transcription factor belongs to APETALA2 (AP2) family and binds to DRE/CRT cis-element and regulates the stress-responsive genes expression independent to abscisic acid (ABA). Utilizing these regulatory genes and elements, generating transgenic plants looks a potential option in administration of abiotic stresses in crop plants. In the present review, role of DREB gene(s) and their expression behavior and transcriptional regulation in response to multiple abiotic stresses in many crop plants including cash crop like sugarcane is narrated, and concomitantly strategizes their implications in stress breeding and transgenic research.

The translational control of oncoprotein expression is implicated in many cancers. Here we report an eIF4A RNA helicase-dependent mechanism of translational control that contributes to oncogenesis and underlies the anticancer effects of silvestrol and related compounds. For example, eIF4A promotes T-cell acute lymphoblastic leukaemia development in vivo and is required for leukaemia maintenance. Accordingly, inhibition of eIF4A with silvestrol has powerful therapeutic effects against murine and human leukaemic cells in vitro and in vivo . We use transcriptome-scale ribosome footprinting to identify the hallmarks of eIF4A-dependent transcripts. These include 5′ untranslated region (UTR) sequences such as the 12-nucleotide guanine quartet (CGG) 4 motif that can form RNA G-quadruplex structures. Notably, among the most eIF4A-dependent and silvestrol-sensitive transcripts are a number of oncogenes, superenhancer-associated transcription factors, and epigenetic regulators. Hence, the 5′ UTRs of select cancer genes harbour a targetable requirement for the eIF4A RNA helicase. The translation of many messenger RNAs that encode important oncogenes and transcription factors depends on the eIF4A RNA helicase to resolve G-quadruplex structures, implying eIF4A inhibition as an effective cancer therapy. eIF4F interaction with oncoproteins The expression of some oncoproteins is regulated at the translational level. Hans-Guido Wendel and colleagues show that a subset of oncoprotein- and transcription factor-encoding mRNAs that are dependent on the translation initiation factor eIF4A contain a G-quadruplex-forming structure in their 5′ untranslated regions. These findings explain why silvestrol, a plant-derived anticancer agent that targets eIF4A-dependent translation, is not generally toxic but can be well tolerated except in cancer cells which are dependent on the activities of these proteins. In a separate study in this issue, Stéphan Vagner and colleagues show that inhibition of eIF4F cooperates with BRAF inhibitors in reducing the growth of melanomas linked to BRAF mutations.

A male patient in his 60s presented with a rare form of hyper-mature senile cataract, characterised by an empty capsular bag in the left eye and diminished vision over 2 years. Initial visual acuity was 20/40 in the right eye and finger counting at one metre in the left eye. A slit lamp examination revealed pseudophakia in the right eye and a fibrosed lens capsule in the left eye. A dilated examination confirmed an empty capsular bag with a fibrosed capsule and normal fundus. Ultrasound findings were anechoic, and anterior segment optical coherence tomography showed an intact lens capsule. The patient underwent intraocular lens implantation (IOL) in the sulcus, resulting in improved visual acuity to 20/32. At the 6-month follow-up, the patient had a stable and well-centred IOL with best corrected visual acuity of 20/20.

Tumor suppressor SMAR1 interacts and stabilizes p53 through phosphorylation at its serine-15 residue. We show that SMAR1 transcription is regulated by p53 through its response element present in the SMAR1 promoter. Upon Doxorubicin induced DNA damage, acetylated p53 is recruited on SMAR1 promoter that allows activation of its transcription. Once SMAR1 is induced, cell cycle arrest is observed that is correlated to increased phospho-ser-15-p53 and decreased p53 acetylation. Further we demonstrate that SMAR1 expression is drastically reduced during advancement of human breast cancer. This was correlated with defective p53 expression in breast cancer where acetylated p53 is sequestered into the heterochromatin region and become inaccessible to activate SMAR1 promoter. In a recent report we have shown that SMAR1 represses Cyclin D1 transcription through recruitment of HDAC1 dependent repressor complex at the MAR site of Cyclin D1 promoter. Here we show that downmodulation of SMAR1 in high grade breast carcinoma is correlated with upregulated Cyclin D1 expression. We also established that SMAR1 inhibits tumor cell migration and metastases through inhibition of TGFbeta signaling and its downstream target genes including cutl1 and various focal adhesion molecules. Thus, we report that SMAR1 plays a central role in coordinating p53 and TGFbeta pathways in human breast cancer.