Carbon dioxide capture has been in the center of interests in the scientific community in recent years because of the implications for global warming, and the development of efficient methods for capturing CO 2 from industrial flue gas has become an important issue. It has been revealed that coordination polymer networks (CPNs) with channels or pores can be applied in gas storage, [1, 2] gas separation, [3] ion exchange, [4] and selective adsorption of organic or inorganic molecules. [1e, 5-7] It has been reported that large amounts of CO 2 can be adsorbed in some CPNs, for example 20 wt % at 195 K and 1 bar in [{Cu(pyrdc)(bpp)} 2 ] n (pyrdc = pyridine-2,3-dicarboxylate, bpp = 1,3-bis(4-pyridyl)propane), [8a] 16 wt % at 298 K and 50 atm in [Cu(dhbc) 2 (4,4'-bpy)] (dhbc = 2,5-dihydroxybenzoate, bpy = bipyridine), [8b] 114 wt % at 195 K and 1 bar in SNU-6, [1c] 150 wt % at 298 K and 42 bar in MOF-177, [9a] and 176 wt % at 303 K and 50 bar in MIL-101c.[9b] However, the selective capture of CO 2 , in particular at ambient temperature and pressure, from industrial emission streams that contain other gases such as N 2 , CH 4 , and H 2 O still remains challenging. [1c, 10, 11] Our approach to selectively capturing CO 2 with porous materials is based on the construction of highly flexible 3D coordination polymer networks whose channels or pores open and close depending on the gas type. Compared to N 2 and H 2 , we expected that CO 2 would interact with the host network more efficiently because of its quadrupole moment (À1.4 10 À39 C m 2 ) and open up channels that are closed for other gases. Our design strategy for flexible 3D networks is to use 2D grids formed from square-planar Ni II macrocyclic complexes as linear linkers [3a, 6, 7a,b, 12] [6] The formation of either 2D or 3D pillared network depends on how the bismacrocyclic complex connects 2D planes (Chart S1 in the Supporting Information), which is affected by the pore size of the 2D layer and the steric hindrance between the pillars. Herein, we report two flexible 3D coordination polymer networks, [(Ni 2 L 2 )(bptc)]·6 H 2 O·3 DEF (1, DEF = N,N-diethylformamide) and [(Ni 2 L 4 )(bptc)]·14 H 2 O (2), which exhibit highly selective CO 2 adsorption over N 2 , H 2 , and CH 4 gases as well as thermal stability up to 300 8C and air and water stability. The CO 2 adsorption isotherms of 1 and 2 show gate opening and closing phenomena as well as hysteretic desorption, which allow efficient CO 2 capture, storage, and sensing. Compounds 1 and 2 are the first 3D pillared networks assembled from Ni II bismacrocyclic complexes. The self-assembly of A and H 4 bptc in DEF/H 2 O/TEA (2:3:0.16, v/v; TEA = triethylamine) yielded violet crystals of 1. The self-assembly of B and Na 4 bptc in DEF/H 2 O (1:4, v/v) afforded 2. Compounds 1 and 2 are insoluble in water and common organic solvents such as MeOH, EtOH, MeCN, chloroform, acetone, toluene, dimethylformamide, and dimethylsulfoxide.In the X-ray crystal structure of 1 (Figure 1), [14]
Dapagliflozin, a new type of drug used to treat diabetes mellitus (DM), is a sodium/glucose cotransporter 2 (SGLT2) inhibitor. Although some studies showed that SGLT2 inhibition attenuated reactive oxygen generation in diabetic kidney the role of SGLT2 inhibition is unknown. We evaluated whether SLT2 inhibition has renoprotective effects in ischemia-reperfusion (IR) models. We evaluated whether dapagliflozin reduces renal damage in IR mice model. In addition, hypoxic HK2 cells were treated with or without SGLT2 inhibitor to investigate cell survival, the apoptosis signal pathway, and the induction of hypoxia-inducible factor 1 (HIF1) and associated proteins. Dapagliflozin improved renal function. Dapagliflozin reduced renal expression of Bax, renal tubule injury and TUNEL-positive cells and increased renal expression of HIF1 in IR-injured mice. HIF1 inhibition by albendazole negated the renoprotective effects of dapagliflozin treatment in IR-injured mice. In vitro, dapagliflozin increased the expression of HIF1, AMP-activated protein kinase (AMPK), and ERK and increased cell survival of hypoxic HK2 cells in a dose-dependent manner. In conclusion, dapagliflozin attenuates renal IR injury. HIF1 induction by dapagliflozin may play a role in renoprotection against renal IR injury.
This paper reports the tensile properties and fracture mechanism of PTB7:PC71BM bulk heterojunction (BHJ) films as a function of composition mixing ratio. An increased concentration of fullerene makes the BHJ films stiffer and more brittle, and fracture occurs along aggregated fullerene domain boundaries. The tensile strength is maximized at a polymer–fullerene content ratio of 1:1. Furthermore, an additive, 1,8-diiodoctane (DIO), in the films induces fine nanomorphology, which increases the stiffness and strength and reduces the ductility of the films further. This is especially true under a high PC71BM load due to the expanded interfacial surface areas between the PC71BM and PTB7 polymer domains. The photovoltaic performance of the BHJ films on polydimethylsiloxane (PDMS) substrates after tensile stretching cycles is also examined in detail.
BackgroundSince hepatocellular carcinoma (HCC) is one of the leading causes of cancer death worldwide, it is still important to understand hepatocarcinogenesis mechanisms and identify effective markers for tumor progression to improve prognosis. Amplification and overexpression of Tropomyosin3 (TPM3) are frequently observed in HCC, but its biological meanings have not been properly defined. In this study, we aimed to elucidate the roles of TPM3 and related molecular mechanisms.MethodsTPM3-siRNA was transfected into 2 HCC cell lines, HepG2 and SNU-475, which had shown overexpression of TPM3. Knockdown of TPM3 was verified by real-time qRT-PCR and western blotting targeting TPM3. Migration and invasion potentials were examined using transwell membrane assays. Cell growth capacity was examined by colony formation and soft agar assays.ResultsSilencing TPM3 resulted in significant suppression of migration and invasion capacities in both HCC cell lines. To elucidate the mechanisms behind suppressed migration and invasiveness, we examined expression levels of Snail and E-cadherin known to be related to epithelial-mesenchymal transition (EMT) after TPM3 knockdown. In the TPM3 knockdown cells, E-cadherin expression was significantly upregulated and Snail downregulated compared with negative control. TPM3 knockdown also inhibited colony formation and anchorage independent growth of HCC cells.ConclusionsBased on our findings, we formulate a hypothesis that overexpression of TPM3 activates Snail mediated EMT, which will repress E-cadherin expression and that it confers migration or invasion potentials to HCC cells during hepatocarcinogenesis. To our knowledge, this is the first evidence that TPM3 gets involved in migration and invasion of HCCs by modifying EMT pathway.
Carbon dioxide capture has been in the center of interests in the scientific community in recent years because of the implications for global warming, and the development of efficient methods for capturing CO 2 from industrial flue gas has become an important issue. It has been revealed that coordination polymer networks (CPNs) with channels or pores can be applied in gas storage, [1, 2] gas separation, [3] ion exchange, [4] and selective adsorption of organic or inorganic molecules. [1e, 5-7] It has been reported that large amounts of CO 2 can be adsorbed in some CPNs, for example 20 wt % at 195 K and 1 bar in [{Cu(pyrdc)(bpp)} 2 ] n (pyrdc = pyridine-2,3-dicarboxylate, bpp = 1,3-bis(4-pyridyl)propane), [8a] 16 wt % at 298 K and 50 atm in [Cu(dhbc) 2 (4,4'-bpy)] (dhbc = 2,5-dihydroxybenzoate, bpy = bipyridine), [8b] 114 wt % at 195 K and 1 bar in SNU-6, [1c] 150 wt % at 298 K and 42 bar in MOF-177, [9a] and 176 wt % at 303 K and 50 bar in MIL-101c. [9b] However, the selective capture of CO 2 , in particular at ambient temperature and pressure, from industrial emission streams that contain other gases such as N 2 , CH 4 , and H 2 O still remains challenging. [1c, 10, 11] Our approach to selectively capturing CO 2 with porous materials is based on the construction of highly flexible 3D coordination polymer networks whose channels or pores open and close depending on the gas type. Compared to N 2 and H 2 , we expected that CO 2 would interact with the host network more efficiently because of its quadrupole moment (À1.4 10 À39 C m 2 ) and open up channels that are closed for other gases. Our design strategy for flexible 3D networks is to use 2D grids formed from square-planar Ni II macrocyclic complexes as linear linkers [3a, 6, 7a,b, 12] and 1,1'-biphenyl-3,3',5,5'tetracarboxylate (bptc 4À ) [13] as a square organic building block, and then to connect the 2D grids with highly flexible alkyl pillars by utilizing alkyl-bridged Ni II bismacrocyclic complexes such as [Ni 2 L 2 ](ClO 4 ) 4 (A) and [Ni 2 L 4 ]-(ClO 4 ) 4 ·8 H 2 O (B, Scheme 1). We previously prepared a 2D pillared bilayer network that behaves like a sponge from other Ni II bismacrocyclic complexes and 1,3,5-benzenetricarboxylate. [6] The formation of either 2D or 3D pillared network depends on how the bismacrocyclic complex connects 2D planes (Chart S1 in the Supporting Information), which is affected by the pore size of the 2D layer and the steric hindrance between the pillars.Herein, we report two flexible 3D coordination polymer networks, [(Ni 2 L 2 )(bptc)]·6 H 2 O·3 DEF (1, DEF = N,N-diethylformamide) and [(Ni 2 L 4 )(bptc)]·14 H 2 O (2), which exhibit highly selective CO 2 adsorption over N 2 , H 2 , and CH 4 gases as well as thermal stability up to 300 8C and air and water stability. The CO 2 adsorption isotherms of 1 and 2 show gate opening and closing phenomena as well as hysteretic desorption, which allow efficient CO 2 capture, storage, and sensing. Compounds 1 and 2 are the first 3D pillared networks assembled from Ni II bismac...
PRF-induced pain relief may be due to temporary blockage of nerve signals through the nerve pathway responsible for reversible neuronal depression. However, CRF-induced pain relief may be due to permanent blockage of nerve signals through other nerve pathways. Therefore, CRF could be applied to chronic inflammatory models used to study the mechanism of neuropathic pain.
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