Two luminescent Zn(II) coordination polymers (CPs) were synthesized under solvothermal condition. CP 1 consists of a 1D chain with the SP 1-periodic net (4,4)(0,2) topology. CP 2 shows 2D (6,3) ...layer. Two CPs are high selectivity and sensitive luminescence sensor of Cr2O72− and Hg2+ ions in water.
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Two new Zn(II) coordination polymers (CPs), {Zn(L)(5-nip)2·5.5H2O}n (1) and {Zn(L)(5-mip)·EtOH}n (2) L = 1,3-bis(benzimidazol-1-yl)-2-propanol, 5-H2nip = 5-nitroisophthalic acid, 5-H2mip = 5-methyisophthalic acid were solvothermally synthesized and characterized by elemental analyses, IR spectra, thermogravimetric analyses, and single-crystal X-ray diffraction. CP 1 possesses a 1D ladder-like chain structure and further packed into 2D supramolecular architectures by π-π stacking interactions. CP 2 exhibits a 2D 63 layer, which is finally extended into 3D supramolecular network via the weak C–H⋯O hydrogen bond interactions. CP 1 and CP 2 can be used as luminescent sensors for Hg2+ and Cr2O72− ions in water.
Background
Diabetic peripheral neuropathy (DPN) is a common neurological complication of diabetes mellitus without efficient interventions. Both lysine demethylase 5B (KDM5B) and sirtuin‐3 (SIRT3) ...have been found to regulate islet function and glucose homeostasis. KDM5B was predicted to bind to the SIRT3 promoter by bioinformatics. Here, we investigated whether KDM5B affected DPN development via modulating SIRT3.
Methods
The db/db mice and high glucose‐stimulated Schwann cells (RSC96) were used as in vivo and in vitro models of DPN, respectively. Glucose level, glucose and insulin tolerance of mice were measured. Neurological function was evaluated by motor nerve conduction velocity (MNCV), tactile allodynia assay and thermal sensitivity assay. Adenosine triphosphate level, oxygen consumption rate, extracellular acidification rate, β‐oxidation rate, acetyl‐CoA level, acetylation levels and activities of long‐chain acyl CoA dehydrogenase (LCAD) and pyruvate dehydrogenase (PDH) were detected. Methyl thiazolyl tetrazolium assay was adopted to determine cell viability. Reactive oxygen species (ROS) production was detected by MitoSox staining. Western blotting for measuring target protein levels. Molecular mechanisms were investigated by co‐immunoprecipitine (Co‐IP), chromatin immunoprecipitation (ChIP) and luciferase reporter assay.
Results
KDM5B was up‐regulated, while SIRT3 was down‐regulated in DPN models. SIRT3 overexpression or AMPK activation ameliorated mitochondrial metabolism dysfunction and ROS overproduction during DPN. KDM5B overexpression triggered mitochondrial metabolism disorder and oxidative stress via directly transcriptional inhibiting SIRT3 expression by demethylating H3K4me3 or indirectly repressing AMPK pathway‐regulated SIRT3 expression.
Conclusion
KDM5B contributes to DPN via regulating SIRT3‐mediated mitochondrial glucose and lipid metabolism. KDM5B inhibition may be an effective intervention for DPN.
Time‐modulated arrays (TMAs) have been widely studied owing to their convenient control mode and simple structure. Although direction‐of‐arrival (DOA) estimation based on TMA has garnered ...considerable attention, underdetermined DOA estimation in TMA is yet to be studied. In this study, a novel method is proposed for underdetermined DOA estimation based on the higher‐order cumulants of harmonic signal in a TMA. The periodic modulation of radio‐frequency switches leads to a TMA generating harmonics in space. Cumulants of harmonic statistics can be used for DOA estimation, and with higher‐order harmonics cumulants, underdetermined DOA estimation can be realised with a TMA using the multiple signal classification method, and the degree of freedom can be improved further. Another advantage of the proposed method is its simple structure, which only requires one receiver with several filters. Numerical simulations show that the proposed method can achieve good resolution and precision performance.
Inflammation is involved in pathogenesis of hypertension. NLRP3 inflammasome activation is a powerful mediator of inflammatory response via caspase-1 activation. The present study was designed to ...determine the roles and mechanisms of NLRP3 inflammasome in phenotypic modulation and proliferation of vascular smooth muscle cells (VSMCs) in hypertension. Experiments were conducted in spontaneously hypertensive rats (SHR) and primary aortic VSMCs. NLRP3 inflammasome activation was observed in the media of aorta in SHR and in the VSMCs from SHR. Knockdown of NLRP3 inhibited inflammasome activation, VSMC phenotypic transformation and proliferation in SHR-derived VSMCs. Increased NFκB activation, histone acetylation and histone acetyltransferase expression were observed in SHR-derived VSMCs and in media of aorta in SHR. Chromatin immunoprecipitation analysis revealed the increased histone acetylation, p65-NFκB and Pol II occupancy at the NLRP3 promoter in vivo and in vitro. Inhibition of NFκB with BAY11-7082 or inhibition of histone acetyltransferase with curcumin prevented the NLRP3 inflammasome activation, VSMC phenotype switching and proliferation in VSMCs from SHR. Moreover, curcumin repressed NFκB activation. Silencing of NLRP3 gene ameliorated hypertension, vascular remodeling, NLRP3 inflammasome activation and phenotype switching in the aorta of SHR. These results indicate that NLRP3 inflammasome activation response to histone acetylation and NFκB activation contributes to VSMC phenotype switching and proliferation and vascular remodeling in hypertension.
It is reported that baicalein can activate PI3K/AKT pathway, inhibit caspase activation and reduce cerebral infarct volume in middle cerebral artery occlusion (MCAO) rats. However, a ...caspase-independent mechanism initiated by poly (ADP-ribose) polymerase-1 (PARP-1) activation has been reported to make more contribution to cells death after ischemic stroke. In the present study, we established a cerebral ischemia/reperfusion (I/R) rat model through middle cerebral artery occlusion following reperfusion to investigate the mechanisms of ischemic tissue recovery following baicalein treatment. The data showed that baicalein treatment at dose of 100 mg/kg for 7 days significantly inhibited the release of cytokines, activation of PARP-1, nuclear translocation of apoptosis-inducing factor (AIF) and macrophage migration inhibitory factor (MIF) in cerebral I/R rats, therefore decreased cerebral infarct volume and neurological scores. Then, we further investigated the signal transduction mechanisms of ischemic tissue protection by baicalein in vitro. Following oxygen and glucose deprivation (OGD) in SH-SY5Y cells, the mitochondrial AIF was translocated into nucleus after 12 h. The co-immunoprecipitation analysis showed that the interaction between AIF and MIF was activated by OGD and subsequently resulted in MIF nuclear translocation. Also, the baicalein inhibited apoptosis, reduced oxidative stress, protected mitochondrial function and restored mitochondrial membrane potential in OGD cells. The results obtained from both in vivo and in vitro study demonstrated the PARP-1/AIF pathway involved in mechanisms of baicalein to protect the cerebral tissues from ischemic injury.
Deregulation of Ubiquitin-conjugating enzyme E2T (UBE2T) contributes to the progression of human cancers. However, its clinical significance and role in hepatocellular carcinoma (HCC) remain unclear. ...Here, we show that UBE2T is up-regulated in HCC and exerts oncogenic activities via ubiquitination of p53. High UBE2T expression was correlated with higher pathological grade, advanced TNM stage, tumor vascular invasion, and poor overall and disease-free survivals in two independent cohorts containing 827 patients with HCC. UBE2T was further identified as an independent factor for overall survival by multivariate analyses. Luciferase reporter assays confirmed that UBE2T was directly targeted by miR-543 which was down-regulated in HCC. In vitro experiments demonstrated that UBE2T overexpression promoted, whereas UBE2T knockdown inhibited HCC cell growth. Ectopic expression of UBE2T resulted in the decreases of p53, p21 and Noxa. Further studies revealed that UBE2T facilitated the degradation of p53 protein via enhancing its ubiquitination. Collectively, our findings suggest UBE2T serves as a promising prognostic factor for HCC and functions as an oncogene. The newly identified miR-543/UBE2T/p53 axis may represent a new potential therapeutic target for HCC intervention.
•UBE2T expression is increased in HCC and correlated with poor outcomes of 827 patients.•UBE2T is targeted by miR-543 in HCC cells.•UBE2T promotes HCC cell growth via facilitating the ubiquitination of p53.
MCC950, an NLRP3 inflammasome inhibitor, displays multiple pharmacological properties. However, the protective potential and underlying mechanism of MCC950 against doxorubicin (DOX)-induced ...myocardial injury has not been well investigated yet. Herein, DOX-induced myocardial injury in mice and in H9c2 myocardial cells was investigated, and the protective effects and underlying mechanism of MCC950 were fully explored. The results showed that MCC950 co-treatment significantly improved myocardial function, inhibited inflammatory and myocardial fibrosis, and attenuated cardiomyocyte pyroptosis in DOX-treated mice. Mechanismly, MCC950 had the potential to inhibit DOX-induced the cleavage of NLRP3, ASC, Caspase-1, IL-18, IL-1β and GSDMD in vivo. Moreover, MCC950 co-treatment in vivo suppressed DOX-induced cytotoxicity as well as inflammatory and cardiomyocyte pyroptosis through the same molecular mechanism. Taken together, our findings validated that MCC950, an NLRP3 inflammasome inhibitor, has the potential to attenuate doxorubicin-induced myocardial injury in vivo and in vitro by inhibiting NLRP3-mediated pyroptosis.
•MCC950 alleviates DOX-induced myocardial dysfunction and inflammation in vivo.•MCC950 attenuates DOX-induced myocardial injury by blocking cardiomyocyte pyroptosis in vivo.•MCC950 inhibits DOX-induced cardiotoxicity in vitro through inhibiting NLRP3-mediated pyroptosis in vitro.
Topological semimetals may have substantial applications in electronics, spintronics, and quantum computation. Recently, ZrTe was predicted as a new type of topological semimetal due to the ...coexistence of Weyl fermions and massless triply degenerate nodal points. In this work, the elastic and transport properties of ZrTe are investigated by combining the first-principles calculations and semiclassical Boltzmann transport theory. Calculated elastic constants prove the mechanical stability of ZrTe, and the bulk modulus, shear modulus, Young's modulus, and Poisson's ratio also are calculated. It is found that spin-orbit coupling (SOC) has slightly enhanced effects on the Seebeck coefficient, which along the a(b) and c directions for pristine ZrTe at 300 K is 46.26 VK−1 and 80.20 VK−1, respectively. By comparing the experimental electrical conductivity of ZrTe (300 K) with the calculated value, the scattering time is determined as 1.59 × 10−14 s. The predicted room-temperature electronic thermal conductivity along the a(b) and c directions is 2.37 Wm − 1 K − 1 and 2.90 Wm − 1 K − 1 , respectively. The room-temperature lattice thermal conductivity is predicted as 17.56 Wm − 1 K − 1 and 43.08 Wm − 1 K − 1 along the a(b) and c directions, showing very strong anisotropy. Calculated results show that isotope scattering produces an observable effect on lattice thermal conductivity. To observably reduce lattice thermal conductivity by nanostructures, the characteristic length should be smaller than 70 nm, based on cumulative lattice thermal conductivity with respect to the phonon mean free path (MFP) at 300 K. It is noted that the average room-temperature lattice thermal conductivity of ZrTe is slightly higher than that of isostructural MoP, which is due to larger phonon lifetimes and smaller Grüneisen parameters. Finally, the total thermal conductivity as a function of temperature is predicted for pristine ZrTe. Our works provide valuable information for ZrTe-based nano-electronics devices, and motivate further experimental works to study elastic and transport properties of ZrTe.
Two new Cd
2+
coordination polymers (CPs), namely {Cd(L)(1,4-PDA)·0.7(C
2
H
5
OH)}
n
(
1
) and {Cd(L)
0.5
(1,8-NDC)·H
2
O}
n
(
2
) L = 1,4-bis(5,6-dimethybenzimidazol-1-yl)-2-butene, 1,4-H
2
PDA = ...1.4-phenylenediacetic acid, 1,8-H
2
NDC = 1,8-naphthalenedicarboxylic acid, were hydrothermally synthesized and characterized.
1
is a (4,4)-layered structure and further extended into a 3D supramolecular network
via
π-π stacking interactions.
2
features a 2D (3,4)-connected
3,4L83
framework.
1
and
2
can act as luminescence sensors for detecting acetylacetone (acac) and Fe
3+
with high sensitivity, selectivity and recyclability. This is the first dual fluorosensors employing CPs for the detection of Fe
3+
and acac. The mechanism for the luminescent sensing of acac and Fe
3+
was suggested.
Two new CPs, namely {Cd(L)(1,4-PDA)·0.7(C
2
H
5
OH)}
n
(
1
) and {Cd(L)
0.5
(1,8-NDC)·H
2
O}
n
(
2
) were fabricated.
1
shows a
sql
2D network.
2
shows a 2D
3,4L83
network. Both
1
and
2
were highly selective and sensitive fluorescent chemosensors toward acetylacetone and Fe
3+
.
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