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Genome-wide identification, evolution involving histone lysine demethylases (KDM) family genes as well as their term in the course of gonadal increase in Nile tilapia.
Lastly, the main metabolite of SER, norsertraline, was detected in the liver, and may also relate to toxicity. This study uncovers mechanisms and key events proposed to lead to impaired behavior and growth after exposure to some antidepressants.Thermochemical transformation of microalgae biomass into graphitic bio-chars entices as proficient bio-adsorbents for heavy metal contaminants. This study explores the synergistic impact of Chlorella sorokiniana on biomass generation and wastewater remediation in high rate algae pond (HRAP). Biomass produced was applied for hydrothermal carbonization-co-liquefaction (HTCL). The structural and morphological characteristics of HTCL products (i.e. bio-chars and bio-oils) have been systematically studied by XRD, Raman, FTIR, elemental analyzer, SEM, BET, and 1H NMR spectroscopy. The crystallite size of the graphite 2H indexing planes was to be 4.65 nm and 14.07 nm in the bio-chars of oiled biomass (MB-OB) and de-oiled biomass (MB-DOB), respectively. The increase in the ID/IG ratio of MB-DOB indicated the highly disordered graphitic structure due to the appearance of carbonyl, hydroxyl, and epoxy functionalities in the line of high C/N and low C/H ratio. Also, the multiple heavy metals remediation of MB-DOB revealed better efficiency as ~100% in 720 min. The kinetics analysis shows the correlation coefficient of pseudo-second-order is well fitted compared to the pseudo-first-order. The Langmuir adsorption model signifies the adsorption of heavy metal ions in a monolayer adsorption manner. The study proposes the microalgae bio-char potential for multiple heavy metals remediation alongside bio-oils.Wax accumulation on the sorghum surface plays an important role in drought tolerance by preventing non-stomatal water loss. Thereby, the effect of post-flowering drought stress (PFDS) on the epicuticular wax (EW) amount, relative water content (RWC), chlorophyll, and grain yield in sorghum drought contrasting genotypes were investigated. The experiment was conducted as a split-plot based on randomized complete block design (RCBD) with two water treatments (normal watering and water holding after 50% flowering stage), and three genotypes (Kimia and KGS23 as drought-tolerant and Sepideh as drought-susceptible). Scanning electron microscopy and GC-MS analyses were used to determine the wax crystals density and its compositions, respectively. In addition, based on literature reviews and publicly available datasets, six wax biosynthesis drought stress-responsive genes were chosen for expression analysis. The results showed that the amounts of EW and wax crystals density were increased in Kimia and Sepideh genotypes and no changed in KGS23 genotype under drought stress. Chemical compositions of wax were classified into six major groups including alkanes, fatty acids, aldehydes, esters, alcohols, and cyclic compounds. Alkanes increment in drought-tolerant genotypes led to make an effective barrier against the drought stress to control water losses. In addition, the drought-tolerant genotypes had higher levels of RWC compared to the drought-susceptible ones, resulted in higher yield produced under drought condition. According to the results, SbWINL1, FATB, and CER1 genes play important roles in drought-induced wax biosynthesis. The results of the present study revealed a comprehensive view of the wax and its compositions and some involved genes in sorghum under drought stress.The entirety of the sediment bed in lake Tyrifjorden, Norway, is contaminated by per- and polyfluoroalkyl substances (PFAS). A factory producing paper products and a fire station were investigated as possible sources. Fire station emissions were dominated by the eight carbon perfluoroalkyl sulfonic acid (PFSA), perfluorooctanesulfonic acid (PFOS), from aqueous film forming foams. Factory emissions contained PFOS, PFOS precursors (preFOS and SAmPAP), long chained fluorotelomer sulfonates (FTS), and perfluoroalkyl carboxylic acids (PFCA). Concentrations and profiles in sediments and biota indicated that emissions originating from the factory were the main source of pollution in the lake, while no clear indication of fire station emissions was found. Ratios of linear-to branched-PFOS increased with distance from the factory, indicating that isomer profiles can be used to trace a point source. A dated sediment core contained higher concentrations in older sediments and indicated that two different PFAS products have been used at the factory, referred to here as Scotchban and FTS mixture. Modelling, based on the sediment concentrations, indicated that 42-189 tons Scotchban, and 2.4-15.6 tons FTS mixture, were emitted. Production of paper products may be a major PFAS point source, that has generally been overlooked. It is hypothesized that paper fibres released from such facilities are important vectors for PFAS transport in the aquatic environment.Anti-apoptotic Bcl-2 critically controls cell death by neutralizing pro-apoptotic Bcl-2-family members at the mitochondria. Bcl-2 proteins also act at the endoplasmic reticulum, the main intracellular Ca2+-storage organelle, where they inhibit IP3 receptors (IP3R) and prevent pro-apoptotic Ca2+-signaling events. IP3R channels are targeted by the BH4 domain of Bcl-2. Some cancer types rely on the IP3R-Bcl-2 interaction for survival. We previously developed a cell-permeable, BH4-domain-targeting peptide that can abrogate Bcl-2's inhibitory action on IP3Rs, named Bcl-2 IP3 receptor disrupter-2 (BIRD-2). This peptide kills several Bcl-2-dependent cancer cell types, including diffuse large B-cell lymphoma (DLBCL) and chronic lymphocytic leukaemia (CLL) cells, by eliciting intracellular Ca2+ signalling. However, the exact mechanisms by which these excessive Ca2+ signals triggered by BIRD-2 provoke cancer cell death remain elusive. Here, we demonstrate in DLBCL that although BIRD-2 activates caspase 3/7 and provokes cell death in a caspase-dependent manner, the cell death is independent of pro-apoptotic Bcl-2-family members, Bim, Bax and Bak. Instead, BIRD-2 provokes mitochondrial Ca2+ overload that is rapidly followed by opening of the mitochondrial permeability transition pore (mPTP). Inhibiting mitochondrial Ca2+ overload using Ru265, an inhibitor of the mitochondrial Ca2+ uniporter complex counteracts BIRD-2-induced cancer cell death. Erastin Finally, we validated our findings in primary CLL patient samples where BIRD-2 provoked mitochondrial Ca2+ overload and Ru265 counteracted BIRD-2-induced cell death. Overall, this work reveals the mechanisms by which BIRD-2 provokes cell death, which occurs via mitochondrial Ca2+ overload but acts independently of pro-apoptotic Bcl-2-family members.
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