Phonon and Raman scattering of two-dimensional transition metal dichalcogenides from monolayer, multilayer to bulk material

Two-dimensional (2D) transition metal dichalcogenide (TMD) nanosheets exhibit remarkable electronic and optical properties. The 2D features, sizable bandgaps, and recent advances in the synthesis, characterization, and device fabrication of the representative MoS$_2$, WS$_2$, WSe$_2$, and MoSe$_2$ TMDs make TMDs very attractive in nanoelectronics and optoelectronics. Similar to graphite and graphene, the atoms within each layer in 2D TMDs are joined together by covalent bonds, while van der Waals interactions keep the layers together. This makes the physical and chemical properties of 2D TMDs layer dependent. In this review, we discuss the basic lattice vibrations of monolayer, multilayer, and bulk TMDs, including high-frequency optical phonons, interlayer shear and layer breathing phonons, the Raman selection rule, layer-number evolution of phonons, multiple phonon replica, and phonons at the edge of the Brillouin zone. The extensive capabilities of Raman spectroscopy in investigating the properties of TMDs are discussed, such as interlayer coupling, spin--orbit splitting, and external perturbations. The interlayer vibrational modes are used in rapid and substrate-free characterization of the layer number of multilayer TMDs and in probing interface coupling in TMD heterostructures. The success of Raman spectroscopy in investigating TMD nanosheets paves the way for experiments on other 2D crystals and related van der Waals heterostructures.Comment: 30 pages, 23 figure

Efficacy of endoluminal interventional therapy in diabetic peripheral arterial occlusive disease: a retrospective trial

<p>Abstract</p> <p>Background</p> <p>The purpose of this study was to assess the efficacy of interventional therapy for peripheral arterial occlusive disease and the difference between diabetic patients and non-diabetic patients.</p> <p>Methods</p> <p>139 consecutive patients between September 2006 and September 2010 who underwent percutaneous lower extremity revascularization for arterial lesions were divided into diabetes group (n = 62) and non-diabetes group (n = 77). Before intervention, rest ankle brachial indexes and three dimensional computed tomography angiography from abdominal aorta to tiptoe were performed. The interventional treatments included angioplasty with or without stenting. The clinical outcomes included rest ankle-brachial indexes, primary patency rates, secondary patency rates and limb-salvage rates for 6-month, 12-month, 24-month and 36-month after treatment. The primary and secondary patency rates of all interventions and the limb-salvage rates of the patients are illustrated by Kaplan-Meier curves and compared by log-rank analysis.</p> <p>Results</p> <p>The interventional operation success rates were 98.4% (61/62) in diabetes group and 100% (77/77) in non-diabetes group. The re-interventional operation success rates were 85.7% (18/21) in diabetes group and 76.9% (20/26) in non-diabetes group. The mean value of ankle brachial indexes was significantly increased after intervention (0.397 ± 0.125 versus 0.779 ± 0.137, t = -25.780, <it>P </it>< 0.001) in diabetes group and (0.406 ± 0.101 versus 0.786 ± 0.121, t = -37.221, <it>P </it>< 0.001) in non-diabetes group. Perioperative 30-day mortality was 0%. Major complications included groin hematoma in 7.2%, and pseudoaneurysm formation 2.2%. In diabetes group, 6, 12, 24, and 36-month primary patency rates were 88.7% ± 4.0%, 62.3% ± 6.6%, 55.3% ± 7.0%, and 46.5% ± 7.5%; secondary patency rates were 93.5% ± 3.1%, 82.3% ± 5.1%, 70.8% ± 6.5%, and 65.7% ± 7%; limb-salvage rates were 95.2% ± 2.7%, 87.7% ± 4.4%, 85.5% ± 4.8%, and 81.9% ± 5.8%. In non-diabetes group, 6, 12, 24, and 36-month primary patency rates were 90.9% ± 3.3%, 71.8% ± 5.4%, 71.8% ± 5.4%, and 60.9% ± 6.2%; secondary patency rates were 96.1% ± 2.2%, 91.6% ± 3.3%, 82.7% ± 4.8%, and 71.8% ± 6.2%; limb-salvage rates were 97.4% ± 1.8%, 94.4% ± 2.7%, 90.6% ± 3.7%, and 83.1% ± 5.4%. The differences between two groups were not significant (<it>P </it>> 0.05).</p> <p>Conclusion</p> <p>With a low risk of morbidity and mortality, the percutaneous revascularization accepted by patients does not affect ultimate necessary surgical revascularization and consequently should be considered as the preferred therapy for chronic lower extremity ischemia. The efficacy and prognosis of interventional therapy in diabetic patients is similar that in non-diabetic patients.</p

Ethyl 7-(4-bromo­phen­yl)-5-trifluoro­methyl-4,7-dihydro­tetra­zolo[1,5-a]pyrimidine-6-carboxyl­ate

In the title compound, C14H11BrF3N5O2, the pyrimidine ring adopts a flattened envelope conformation with sp 3-hybridized carbon as the flap [deviation = 0.177 (3) Å]. The dihedral angle between tetra­zole and bromo­phenyl rings is 84.3 (1)°. In the crystal, mol­ecules are linked into centrosymmetric dimers by pairs of N—H⋯N hydrogen bonds

5′-Amino-2-oxo-2′,3′-dihydro­spiro­[indoline-3,7′-thieno[3,2-b]pyran]-6′-carbonitrile 1′,1′-dioxide

In the title compound, C15H11N3O4S, the dihedral angle between the mean planes of the dihydro­indol-2-one (r.m.s. deviation = 0.015 Å) and dihydro­thieno[3,2-b]pyran (r.m.s. deviation = 0.011 Å) ring systems is 89.53 (3)°. The crytal packing is consolidated by inter­molecular N—H⋯O and N—H⋯N hydrogen bonds, which link the mol­ecules into a two-dimensional network into sheets lying parallel to (100)

Poly[aqua­(μ2-oxalato)(4-oxidopyri­din­ium)erbium(II)]

The title complex, [Er(C5H5NO)(C2O4)(H2O)]n, is a new erbium polymer based on oxalate and 4-oxidopyridinium ligands. The ErII center is coordinated by six O atoms from three oxalate ligands, one O atom from a 4-oxidopyridinium ligand and one water mol­ecule, and displays a distorted square-anti­prismatic coordination geometry. The oxalate ligands are both chelating and bridging, and link ErII ions, forming Er–oxalate layers in which the attached water and 4-oxidopyridinium units point alternately up and down. A mirror plane passes through the Er atom, one C, the oxide O and two oxalate O atoms. The layers are assembled into a three-dimensional supra­molecular network via inter­molecular hydrogen bonding and π–π stacking inter­actions [centroid–centroid distances of 3.587 (2) Å between parallel pyridinium rings]. Both the water mol­ecule and the 4-oxidopyridinium ligand are disordered over two sites in a 1:1 ratio

5-Amino-7-(3-chloro­phen­yl)-3,7-di­hydro-2H-thieno[3,2-b]pyran-6-carbo­nitrile 1,1-dioxide

The title compound, C14H11ClN2O3S, with fused thiophene and pyran rings, was synthesized via the condensation of dihydro­thio­phen-3(2H)-one 1,1-dioxide and 2-(3-chloro­benz­yl­idene)malononitrile catalysed by triethyl­amine in ethanol. The thio­phene ring adopts an envelope conformation and the pyran ring is planar (r.m.s. deviation = 0.0067 Å). The dihedral angle between the pyran and phenyl rings is 80.8 (1)°. The crystal packing is stabilized by inter­molecular N—H⋯N and N—H⋯O hydrogen bonds in which the cyano N and sulphone O atoms, respectively, acting as acceptors

Inhibition of Notch1 reverses EMT and chemoresistance to cisplatin via direct downregulation of MCAM in triple-negative breast cancer cells

Resistance to chemotherapy continues to be a critical issue in the clinical therapy of triple-negative breast cancer (TNBC). Epithelial-mesenchymal transition (EMT) is thought to contribute to chemoresistance in several cancer types, including breast cancer. Identification of the key signaling pathway that regulates the EMT program and contributes to chemoresistance in TNBC will provide a novel strategy to overcome chemoresistance in this subtype of cancer. Herein, we demonstrate that Notch1 positively associates with melanoma cell adhesion molecule (MCAM), a unique EMT activator, in TNBC tissue samples both at mRNA and protein levels. High expression of Notch1 and MCAM both predicts a poor survival in basal-like/TNBC patients, particularly in those treated with chemotherapy. The expression of Notch1 and MCAM in MDA-MB-231 cells gradually increases in a time-dependent manner when exposing to low dose cisplatin. Moreover, the expressions of Notch1 and MCAM in cisplatin-resistant MDA-MB-231 cells are significantly higher than wild-type counterparts. Notch1 promotes EMT and chemoresistance, as well as invasion and proliferation of TNBC cells via direct activating MCAM promoter. Inhibition of Notch1 significantly downregulates MCAM expression, resulting in the reversion of EMT and chemoresistance to cisplatin in TNBC cells. Our study reveals the regulatory mechanism of the Notch1 pathway and MCAM in TNBC and suggesting that targeting the Notch1/MCAM axis, in conjunction with conventional chemotherapies, might be a potential avenue to enhance the therapeutic efficacy for patients with TNBC

MicroRNA-203 inhibits cell proliferation by repressing ΔNp63 expression in human esophageal squamous cell carcinoma

<p>Abstract</p> <p>Background</p> <p>This study was performed to investigate the effect of microRNA-203 (miR-203) and ΔNp63 on cell proliferation and the functional connection between miR-203 and ΔNp63 in ESCC.</p> <p>Methods</p> <p>We employed 2 human ESCC cell lines, Eca109 and TE-1, as the model system. The effect of miR-203 and ΔNp63 on cell proliferation was determined in cells transfected with miR-203 mimic and ΔNp63 small interfering RNA (siRNA), respectively. The regulation of ΔNp63 expression in ESCC cells by miR-203 was studied by luciferase reporter assay, RT-PCR and western blot analysis in cells transfected with miR-203. The effect of ΔNp63 re-expression on miR-203 induced inhibition of cell proliferation was studied by cell proliferation assay in cells cotransfected with miR-203 and pcDNA-ΔNp63 plasmid (without the 3'-UTR of <it>ΔNp63</it>).</p> <p>Results</p> <p>We found that both miR-203 and ΔNp63 siRNA signicantly inhibited cell proliferation in ESCC. MiR-203 could down-regulate endogenous ΔNp63 expression at the posttranscriptional level. Moreover, re-expression of ΔNp63 in cells transfected with miR-203 significantly attenuated the miR-203 induced inhibition of cell proliferation.</p> <p>Conclusions</p> <p>Our data implied that miR-203 could inhibit cell proliferation in human ESCC through ΔNp63-mediated signal pathway. Therefore, we propose that miR-203 might be used as a therapeutic agent for human ESCC.</p