16 research outputs found
Microporous Organic Network: Superhydrophobic Coating to Protect Metal–Organic Frameworks from Hydrolytic Degradation
Despite
the rapid development of versatile metal–organic
frameworks (MOFs), the synthesis of water-stable MOFs remains challenging,
which significantly limits their practical applications. Herein, a
novel engineering strategy was developed to prepare superhydrophobic
MOFs by an in situ fluorinated microporous organic
network (FMON) coating. Through controllable modification, the resulting
MOF@FMON retained the porosity and crystallinity of the pristine MOFs.
Owing to the superhydrophobicity of the FMON and the feasibility of
MOF synthesis, the FMON coating could be in situ integrated
with various water-sensitive MOFs to provide superhydrophobicity.
The coating thickness and hydrophobicity of the MOF@FMON composites
were easily regulated by changing the FMON monomer concentration.
The MOF@FMON composites exhibited excellent oil/water separation and
catalytic activities and enhanced durability in aqueous solutions.
This study provides a general approach for the synthesis of superhydrophobic
MOFs, expanding the application scope of MOFs
Immunofluorescent staining of TRPV1 and analysis of its expression pattern in DRG neurons at varying time points after the establishment of DMA.
<p><b>A–E</b>, representative photographs of TRPV1 staining in DRG of different groups. <b>F</b>, illustration of the percentage of TRPV1-IR neurons over total neurons in vehicle, DMA 7 d, 14 d, 21 d and 28 d group (n = 4–6). <b>G</b>, histogram for size distribution of TRPV1-IR neurons. Note the decreased distribution of TRPV1 in neurons with cross-sectional area larger than 400–500 and increased distribution of this protein within the range of 100–400 µm<sup>2</sup> (n = 4–6). <b>H</b>, comparison of the optical density due to TRPV1 immunostaining in small-sized (100–500 µm<sup>2</sup>) and medium-sized (500–1200 µm<sup>2</sup>) DRG neurons of different groups (n = 4–6). *<i>P</i><0.05, **<i>P</i><0.01 <i>vs</i>. vehicle control. Scale bar  = 100 µm.</p
Immunofluorescent staining of TRPV1 in plantar skin of hind paw with the progression of DMA.
<p>A–E, typical photograsph of TRPV1 immunoreactivities in vehicle and DMA model rats at varied time points. A′–C′, the magnified pictures from the rectangle areas in A–C. F, optical density analysis of TRPV1 immunoreactivities in epidermis and dermis displaying strong enhancement on DMA 7 d and 14 d. Sc, Ep and De are the abbreviation of stratum corneum, epidermis and dermis, respectively. Scale bar  = 20 µm</p
Percentage of NF200-, IB4- and CGRP-IR neurons in vehicle-treated and DMA 14 d groups (n = 4–6).
<p>*<i>P</i><0.05, **<i>P</i><0.01 <i>vs</i>. vehicle group.</p
Immunofluorescent staining of TRPV1 in spinal dorsal horn (SDH) with the progression of DMA.
<p><b>A–E</b>, representative photographs of TRPV1 staining in SDH in vehicle, DMA 7 d, 14 d, 21 d and 28 d groups. <b>F</b>, optical density analysis of TRPV1 staining in SDH showing the increased TRPV1-IR neurons on DMA 7 d and 14 d group (n = 4–6). Scale bar  = 100 µm.</p
DM and DMA rat model induced by STZ injection.
<p>Time course of blood glucose concentration (<b>A</b>), body weight (<b>B</b>) and paw withdrawal threshold (<b>C</b>) alterations after STZ or citrate buffer (vehicle) treatment. Data are presented as meanS.E.M. (n = 30), **<i>P</i><0.01 <i>vs</i>. vehicle control.</p
Single intrathecal application of TRPV1 antagonists alleviates mechanical allodynia and thermal hyperalgesia.
<p><b>A</b> and <b>B</b>, single application of RR and CPZ at varing doses caused differential inhibition of mechanical sensitivity of DMA rats. <b>C</b>, single application of RR and CPZ at high dose caused significant inhibition of thermal hyperalgesia in DM rats. *<i>P</i><0.05, **<i>P</i><0.01 <i>vs</i>. vehicle control of the same time. <sup>#</sup><i>P</i><0.05, <sup>##</sup><i>P</i><0.01 <i>vs</i>. drugs of middle dose.</p
Double labeling rate of TRPV1 immunoreactivity with that of NF200, CGRP or IB4 in DRG neurons (n = 4–6).
<p>*<i>P</i><0.05 <i>vs</i>. vehicle group.</p
Multiple intrathecal applications of TRPV1 antagonists cumulatively antagonize mechanical allodynia.
<p><b>A</b> and <b>B</b>, long-term effects of multiple applications of ruthenium red and capsazepine for consecutive 7 days (n = 6). <b>C</b> and <b>D</b>, reconstruction of the decay response diagram from <b>A</b> and <b>B</b> after the withdrawal of RR (<b>A</b>) and CPZ (<b>B</b>) (n = 6).The value in longitudinal axis was normalized by the thresholds value on DMA 20 d. The linear regressions were performed to calculate the decay rates and to evaluate the half decay times (‘Decay<sub>50</sub>’), and the results are shown above the plots. *<i>P</i><0.05, **<i>P</i><0.01 <i>vs</i>. vehicle control of the same time. <sup>#</sup><i>P</i><0.05, <sup>##</sup><i>P</i><0.01 <i>vs</i>. drugs of middle dose.</p
i.t. Dex and Ropi combinations dose-dependently inhibited CFA-induced thermal hyperalgesia of the injected hind paw.
<p>i.t. Dex and Ropi combinations dose-dependently prolonged analgesia duration (<b>A</b>). Iosobologram for combination analgesia was shown in <b>B</b>. The AUCs for different groups were calculated to perform statistical analysis (<b>C</b>). The dose-effect or log (dose)-effect curves for combination analgesic effects were shown in <b>D</b> and <b>E</b>. * <i>p</i><0.05; *** <i>p</i><0.001, compared with CFA-Veh group; arrows indicated s.c. CFA injection and i.t. intervention time point, respectively.</p