11 research outputs found

    Efficient SO<sub>2</sub> Absorptions by Four Kinds of Deep Eutectic Solvents Based on Choline Chloride

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    Four kinds of deep eutectic solvents (DESs) based on choline chloride (ChCl) with ethylene glycol (EG), malonic acid (MA), urea, and thiourea as hydrogen bond donors were prepared and characterized. All these DESs show good thermal stability and can be stable at 363 K, which is beneficial for the application in flue gas desulfurization. Then, SO<sub>2</sub> absorption capacities of these DESs were determined at different temperatures and SO<sub>2</sub> partial pressures. The absorption results demonstrate that ChCl–EG (1:2) and ChCl–thiourea (1:1) DESs exhibit excellent absorption performances, and the absorption capacities are 2.88 and 2.96 mol SO<sub>2</sub> per mol DES at 293 K and 1 atm, respectively. In addition, the SO<sub>2</sub> absorption and regeneration experiments were conducted. All solvents can be regenerated at 343 K with N<sub>2</sub> bubbling, and the absorption capacities of DESs remain without a significant loss after six absorption and desorption cycles. What’s more, the absorption mechanism of SO<sub>2</sub> in these DESs were investigated by IR and <sup>1</sup>H NMR

    Solubility of Dilute SO<sub>2</sub> in Mixtures of <i>N</i>,<i>N</i>‑Dimethylformamide + Polyethylene Glycol 400 and the Density and Viscosity of the Mixtures

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    In this work, the isothermal gas–liquid equilibrium (GLE) data were measured for the system of polyethylene glycol 400 (PEG 400) + <i>N</i>,<i>N</i>-dimethylformamide (DMF) + SO<sub>2</sub> + N<sub>2</sub> at 308.15 K and 123 kPa with SO<sub>2</sub> partial pressures in the range of (16.8 to 115) Pa. The Henry’s law constant (<i>H</i>′) and standard Gibbs free energy change (Δ<i>G</i>) were calculated from these GLE data. Furthermore, the densities and viscosities of binary mixtures of DMF + PEG 400 were also measured over the whole concentration range at <i>T</i> = (298.15 to 313.15) K. From the experimental data, including density and viscosity values, the excess molar volumes (<i>V</i><sub>m</sub><sup>E</sup>), and viscosity deviations (Δη), the calculated results are fitted to a Redlich–Kister equation to obtain the coefficients and estimate the standard deviations between the experimental and the calculated quantities

    Solute Carrier Family 26 Member a2 (<i>slc26a2</i>) Regulates Otic Development and Hair Cell Survival in Zebrafish

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    <div><p>Hearing loss is one of the most prevalent human birth defects. Genetic factors contribute to the pathogenesis of deafness. It is estimated that one-third of deafness genes have already been identified. The current work is an attempt to find novel genes relevant to hearing loss using guilt-by-profiling and guilt-by-association bioinformatics analyses of approximately 80 known non-syndromic hereditary hearing loss (NSHL) genes. Among the 300 newly identified candidate deafness genes, slc26a2 were selected for functional studies in zebrafish. The slc26a2 gene was knocked down using an antisense morpholino (MO), and significant defects were observed in otolith patterns, semicircular canal morphology, and lateral neuromast distributions in morphants. Loss-of-function defects are caused primarily by apoptosis, and morphants are insensitive to sound stimulation and imbalanced swimming behaviours. Morphant defects were found to be partially rescued by co-injection of human SLC26A2 mRNA. All the results suggest that bioinformatics is capable of predicting new deafness genes and this showed slc26a2 is to be a critical otic gene whose dysfunction may induce hearing impairment.</p></div

    <i>slc26a2</i> knockdown in wild-type embryos and rescue of <i>slc26a2</i> overexpression in S2-SP1 morphants.

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    <p>(A) Variations in otolith size of morphant (S2-SP1 knockdown) embryos were observed at 72hpf. Based on the otolith size, malformed embryos were classified as type A (abnormal phenotype, including small, tiny, fused and misplaced otoliths) or type B (abnormal number of otoliths, including increased and decreased otoliths). (B) Morphology of 72hpf WT embryos injected with different morpholinos. One or two cell embryos were injected with 4 ng of S2-SP1 or Mcon. WT. Note the change in otolith size. (C) Schematic representation of two functional domains of zebrafish and human <i>slc26a2</i> proteins. Degree of identity/similarity indicated for the sulphate transporter, STAS, and the C terminal dimerization domains. (D) Relative numbers of embryos in each category. Single-celled embryos were injected with indicated morpholinos at the indicated dose and categorized at 72hpf. Single-celled S2-SP1 embryos were either uninjected or were injected with 150 pg of human <i>SLC26A2</i> mRNA and categorized at 72 hpf. (N = number of observed embryos).</p

    Guilt-by-profiling and guilt-by-association point selection method for a given function probability value calculation.

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    <p>Guilt-by-association sorting is based on gene function contact (FL). Each FL division has a weight value and some probability that two genes annotated with the same GO pathway. GO annotations are classified within a given range. All 12 categories of GO pathways produced specific FL maps and each FL map corresponded to at least one diagram with these GO branches: (A) biological processes, (B) cellular components, and (C) molecular functions. We scored combinations of specific genes and GO annotations using the FL map. (D) Guilt-by-profiling and guilt-by-association algorithm scores were obtained using a logistic regression model combined with free parameters.</p

    <i>slc26a2</i> mRNA expression in embryonic and adult zebrafish.

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    <p>(A)RT-PCR analysis of <i>slc26a2</i> expression in 0–96 h zebrafish yielded 405 bp products, GAPDH served as an internal control for cDNA quantification and gave a 275 bp product. mRNA expression of <i>slc26a2</i> was detected in the first development period, and transcription remained high after 48 h. (B) Expression of <i>slc26a2</i> in WT embryos at 12 and 26hpf, detected by in situ hybridization, at 12hpf. The <i>slc26a2</i> transcript was expressed broadly, and at 26hpf, <i>slc26a2</i> was expressed circumferentially around the ln, lateral line primordium; ot, otic vesicle; pf, pectoral fin, and mb, midbrain. This suggests a function for slc26a2 in the inner ear and neuromast development. Wild insets depict enlarged images of the otic vesicles and lateral neuromasts. (C) RT-PCR confirmed the effectiveness of S2-SP1, and specific products were amplified from cDNA. Wild-type zebrafish yielded 1256 bp products for <i>slc26a2</i>, and morphants had 516 bp products for S2-SP1 in addition to those observed in WT fish. Two bands appeared for morphants but only one band was seen for WT.</p

    Knockdown of <i>slc26a2</i> induces semicircular canal defects in larval zebrafish.

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    <p>(A) Changes in semicircular canal morphology and cilia size (scale bars = 30 μm). (B) Changes of neuromasts numbers and hair cell numbers in lateral line (scale bars = 20 μm). (C, D) Changes of cilia numbers in the inner ear (scale bars = 20 μm). (D) Statistical analysis of the ciliary bundles in the inner ear in different types of embryos at 120hpf, including wild type(WT), mismatch-MO control, S2-SP1 MO and Rescue. (E) Statistical analysis of the L1-8 neuromasts numbers in the posterior lateral line in different types of embryos at 120hpf, including WT, Mis-con, S2-SP1 and Rescue. (F) Statistical analysis of the hair cells numbers per neuromast in different types of embryos at 120hpf, including WT, Miscon, S2-SP1 and Rescue. ***<i>P</i><0.001.</p

    Knockdown of <i>slc26a2</i> induces apoptotic signals.

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    <p>Morphology of 120hpf WT AB line zebrafish embryos injected with morpholinos. One- or two-celled embryos were injected with 4 ng of S2-SP1 and Mcon MO (control). WT was injected with RNase-free water. Neuromast hair cells were measured with TUNEL and changes in apoptotic signals in the anterior and posterior lateral neuromasts occurred (scale bars = 10 μm). (B) Statistical analysis of the apoptotic hair cells in anterior and posterior lateral neuromasts in different types of embryos at 120hpf, including WT, S2-SP1 and Rescue, in order to exclude the possibility that the apoptosis hair cells of MO knockdown zebrafish were due to off-target MO toxicity, we co-injected S2-SP1 with p53-MO. ***P<0.001.</p

    Zebrafish or human mRNA co-injection rescues the numbers of neuromasts, hair cells per neuromast and cilia per neuromast in morphants.

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    <p>The rescue experiments are performed by co-injecting S2-SP1 with SLC26A2 mRNA or slc26a2 mRNA, and the numbers of neuromasts, hair cells per neuromast and cilia per neuromast in the rescued embryos are all increased compared with S2-SP1 morphants alone. Neuromasts, hair cells and cilia were detected in 120hpf Tg (Brn3c:mGFP) transgenic zebrafish larvae. The average L1-L8 neuromasts of 120hpf zebrafish was 4.6 ± 0.4 for S2-SP1 zebrafish, while 7.6 ± 0.5 for S2-SP1+SLC26A2 mRNA, 7.8 ± 0.3 for S2-SP1+slc26a2 mRNA. Numbers of hair cells per neuromast both in anterior and posterior line in S2-SP1 knockdown 120hpf larvae were 4.5±0.5 less than in 120hpf zebrafish were 13.0 ±1.0 for S2-SP1+SLC26A2 mRNA and for S2-SP1+slc26a2 mRNA were 13.5 ± 0.5. And numbers of cilia in morphants were 6.6 ± 0.5 less than in 120hpf zebrafish were 11.5 ±0.5 for S2-SP1+SLC26A2 mRNA and for S2-SP1+slc26a2 mRNA were 13 ± 1. Statistical analysis of numbers of neuromasts, hair cells per neuromast and cilia in different types of embryos at 120hpf, including S2-SP1, S2-SP1+SLC26A2 mRNA and S2-SP1+slc26a2 mRNA. ***P<0.001.</p
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