Theoretical Study of Mechanism and Dynamics on Reaction of (CH₃)₂NH with CH₃

The mechanism and dynamics for the bimolecular reaction of (CH₃)₂NH with CH₃ have been investigated based on the G3//MP2/6-311G­(<i>d</i>,<i>p</i>) level of theory. Our calculations show that when the two reactants approach each other, three prereaction complexes, RC1, RC2, and RC3, can be formed through van der Waals force or hydrogen bonding. From RC1, RC2, and RC3, six routes have been established. Among the six routes, the two routes (R1 and R2) from van der Waals prereaction complex RC1 are the main routes for the title reaction. R1 and R2 are hydrogen abstractions routes associated with H_N and H_Cα atoms in DMA, respectively. The calculated energy barriers for R1 and R2 are 12.3 and 13.7 kcal/mol, respectively. Both the potential energy surfaces of R1 and R2 locate a “reactant-like” transition state, as well as van der Waals complexes before and after the transition state. The slight preference of R1 over R2 might be related to the higher similarity between the structures of RC1 and the transition state for R1 (TS1), namely, the structure of TS1 is more “reactant-like”. The rate constants of the two favorable H abstraction reaction routes, R1 and R2, are evaluated over a wide temperature range of 200–3000 K by the variational transition state theory (VTST) methods, which can be expressed as <i>k</i>_R1 = 5.30 × 10^–13(<i>T</i>/1000)^3.0 exp­(−2883/<i>T</i>) cm³ molecule^–1 s^–1 and <i>k</i>_R2 = 8.34 × 10^–13(<i>T</i>/1000)^4.5 exp­(−3100/<i>T</i>) cm³ molecule^–1 s^–1, respectively. The predicted rate constant of the H_N abstraction (route R1) is in good agreement with the available experimental data

On the Potential of Using the Al₇ Superatom as an Excess Electron Acceptor To Construct Materials with Excellent Nonlinear Optical Properties

With the aid of density functional theory (DFT) calculations, we found that, when alkali metal approaches the Al₇ superatom, its outermost s-value electron can be trapped by Al₇ to give the superatom compound MAl₇ (M = Li, Na, K) with an excess electron. Different analyses including natural bond orbital (NBO), electron localization function (ELF), and energy decomposition analysis (EDA) show that the resulting M–Al bond is strong and has a polar covalent character. The optimizations of self-assemblies (MAl₇)_<i>n</i> (<i>n</i> = 2, 3) have been performed to explore the stability of MAl₇ in the solid state. The results reveal that only NaAl₇ can keep its structural integrity as a building block upon self-assembling, while serious aggregations between Al₇ clusters occur in the dimers and trimers of LiAl₇ and KAl₇, despite the fact that the Li–Al₇ and K–Al₇ bond energies are comparable to that of Na–Al₇. Born–Oppenheimer molecular dynamics (BOMD) simulations for (NaAl₇)_<i>n</i> (<i>n</i> = 2, 3) indicate that these species are stable toward fragmentation at 300 K. The β₀ values of (NaAl₇)_<i>n</i> (<i>n</i> = 1, 2, and 3) predicted at the CAM-B3LYP/6-311+G­(3df) level of theory are in the range of 1.6 × 10⁴a.u. to 7.5 × 10⁴ a.u.. This theoretical study implies that NaAl₇ is a promising candidate for nolinear optical (NLO) materials. We provide theoretical evidence for the possibility of using the Al₇ superatom as an excess electron acceptor to construct materials with excellent NLO properties. Further experimental research is invited

Empirical Mass and Kinetic Models for the Flash Evaporation of NaCl–Water Solution

This paper attempts to provide empirical mass and kinetic models for the flash evaporation of sodium chloride (NaCl) aqueous solution based on experimental phenomena. The models have nine parameters and six affecting factors including initial temperature, operation pressure, NaCl mass fraction, solution depth, evaporator diameter and time. On the basis of a large number of flash evaporation experimental data from various literatures, the mass model parameters were optimized and validated. After optimization of the model parameters with 283 sets of literature experimental data, the average relative error between the model values and the experimental data is about 5.7%. And a statistical method proved the mass model is well posed. The verification with other 215 sets of literature experimental data showed the mass model is in good agreement with flash evaporation phenomena, and the average relative error between the model values and the experimental data is about 8.3%. Then, the kinetic model of flash evaporation was obtained according to the empirical mass model. Finally, the analysis of these models indicated that the increase of initial temperature or evaporator diameter and the decrease of operating pressure are in favor of evaporation. Although the increase of solution depth can improve the evaporated mass, the corresponding evaporation efficiency will be slightly reduced. And the increase of salt content is having a detrimental effect on the evaporation of NaCl–water solution. In addition, the influence of salt content on evaporation at higher operating pressure is more obvious than that at lower operating pressure. The above results show that these models proposed in our work have high accuracy, wide practicability, and good rationality

The Quest for Metal–Metal Quadruple and Quintuple Bonds in Metal Carbonyl Derivatives: Nb₂(CO)₉ and Nb₂(CO)₈

The synthesis by Power and co-workers of the first metal–metal quintuple bond (<i>Science</i> <b>2005</b>, <i>310</i>, 844) is a landmark in inorganic chemistry. The 18-electron rule suggests that Nb₂(CO)₉ and Nb₂(CO)₈ are candidates for binary metal carbonyls containing metal–metal quadruple and quintuple bonds, respectively. Density functional theory (MPW1PW91 and BP86) indeed predicts structures having very short Nb–Nb distances of ∼2.5 Å for Nb₂(CO)₉ and ∼2.4 Å for Nb₂(CO)₈ as well as relatively large Nb–Nb Wiberg bond indices supporting these high formal Nb–Nb bond orders. However, analysis of the frontier molecular orbitals of these unbridged structures suggests formal NbNb triple bonds and 16-electron metal configurations. This contrasts with an analysis of the frontier orbitals in a model chromium­(I) alkyl linear CH₃CrCrCH₃, which confirms the generally accepted presence of chromium–chromium quintuple bonds in such molecules. The presence of NbNb triple bonds rather than quadruple or quintuple bonds in the Nb₂(CO)_<i>n</i> (<i>n</i> = 9, 8) structures frees up d­(<i>xy</i>) and d­(<i>x</i>²–<i>y</i>²) orbitals for dπ→pπ* back-bonding to the carbonyl groups. The lowest energy Nb₂(CO)_<i>n</i> structures (<i>n</i> = 9, 8) are not these unbridged structures but structures having bridging carbonyl groups of various types and formal Nb–Nb orders no higher than three. Thus, the two lowest energy Nb₂(CO)₉ structures have NbNb triple bond distances of ∼2.8 Å and three semibridging carbonyl groups, leading to a 16-electron configuration rather than an 18-electron configuration for one of the niobium atoms. The lowest energy structure of the highly unsaturated Nb₂(CO)₈ is unusual since it has a formal <i>single</i> Nb–Nb bond of length ∼3.1 Å and two four-electron donor η²-μ-CO groups, thereby giving each niobium atom only a 16-electron configuration

Construction of the Tetrahedral Trifluorophosphine Platinum Cluster Pt₄(PF₃)₈ from Smaller Building Blocks

The experimentally known but structurally uncharacterized Pt₄(PF₃)₈ is predicted to have an <i>S</i>₄ structure with a central distorted Pt₄ tetrahedron having four short PtPt distances, two long Pt–Pt distances, and all terminal PF₃ groups. The structures of the lower nuclearity species Pt­(PF₃)_<i>n</i> (<i>n</i> = 4, 3, 2), Pt₂(PF₃)_<i>n</i> (<i>n</i> = 7, 6, 5, 4), and Pt₃(PF₃)₆ were investigated by density functional theory to assess their possible roles as intermediates in the formation of Pt₄(PF₃)₈ by the pyrolysis of Pt­(PF₃)₄. The expected tetrahedral, trigonal planar, and linear structures are found for Pt­(PF₃)₄, Pt­(PF₃)₃, and Pt­(PF₃)₂, respectively. However, the dicoordinate Pt­(PF₃)₂ structure is bent from the ideal 180° linear structure to approximately 160°. Most of the low-energy binuclear Pt₂(PF₃)_<i>n</i> (<i>n</i> = 7, 6, 5) structures can be derived from the mononuclear Pt­(PF₃)_<i>n</i> (<i>n</i> = 4, 3, 2) structures by replacing one of the PF₃ groups by a Pt­(PF₃)₄ or Pt­(PF₃)₃ ligand. In some of these binuclear structures one of the PF₃ groups on the Pt­(PF₃)_<i>n</i> ligand becomes a bridging group. The low-energy binuclear structures also include symmetrical [Pt­(PF₃)_<i>n</i>]₂ dimers (<i>n</i> = 2, 3) of the coordinately unsaturated Pt­(PF₃)_<i>n</i> (<i>n</i> = 3, 2). The four low-energy structures for the trinuclear Pt₃(PF₃)₆ include two structures with central equilateral Pt₃ triangles and two structures with isosceles Pt₃ triangles and various arrangements of terminal and bridging PF₃ groups. Among these four structures the lowest-energy Pt₃(PF₃)₆ structure has an unprecedented four-electron donor η²-μ₃-PF₃ group bridging the central Pt₃ triangle through three Pt–P bonds and one Pt–F bond. Thermochemical studies on the aggregation of these Pt-PF₃ complexes suggest the tetramerization of Pt­(PF₃)₂ to Pt₄(PF₃)₈ to be highly exothermic regardless of the mechanistic details

DataSheet5_Role and mechanism of NCAPD3 in promoting malignant behaviors in gastric cancer.ZIP

Background:Gastric cancer (GC) is one of the major malignancies threatening human lives and health. Non-SMC condensin II complex subunit D3 (NCAPD3) plays a crucial role in the occurrence of many diseases. However, its role in GC remains unexplored.Materials and Methods:The Cancer Genome Atlas (TCGA) database, clinical samples, and cell lines were used to analyze NCAPD3 expression in GC. NCAPD3 was overexpressed and inhibited by lentiviral vectors and the CRISPR/Cas9 system, respectively. The biological functions of NCAPD3 were investigated in vitro and in vivo. Gene microarray, Gene set enrichment analysis (GSEA) and ingenuity pathway analysis (IPA) were performed to establish the potential mechanisms.Results:NCAPD3 was highly expressed in GC and was associated with a poor prognosis. NCAPD3 upregulation significantly promoted the malignant biological behaviors of gastric cancer cell, while NCAPD3 inhibition exerted a opposite effect. NCAPD3 loss can directly inhibit CCND1 and ESR1 expression to downregulate the expression of downstream targets CDK6 and IRS1 and inhibit the proliferation of gastric cancer cells. Moreover, NCAPD3 loss activates IRF7 and DDIT3 to regulate apoptosis in gastric cancer cells.Conclusion:Our study revealed that NCAPD3 silencing attenuates malignant phenotypes of GC and that it is a potential target for GC treatment.</p

Cyclization of Thiocarbonyl Groups in Binuclear Homoleptic Nickel Thiocarbonyls To Give Ligands Derived from Sulfur Analogues of Croconic and Rhodizonic Acids

The sulfur analogue of the well-known Ni­(CO)₄, namely, Ni­(CS)₄, has been observed spectroscopically in low temperature matrices but is not known as a stable species under ambient conditions. Theoretical studies show that Ni­(CS)₄ with monomeric CS ligands and tetrahedrally coordinated nickel is disfavored by ∼17 kcal/mol relative to unusual isomeric Ni­(C₂S₂)₂ structures. In the latter structures the CS ligands couple pairwise through C–C bond formation to give dimeric SCCS ligands, which bond preferentially to the nickel atom through their CS bonds rather than their CC bonds. Coupling of CS ligands in the lowest energy binuclear Ni₂(CS)_<i>n</i> (<i>n</i> = 7, 6, 5) structures results in cyclization to give remarkable C_<i>n</i>S_<i>n</i> (<i>n</i> = 5, 6) ligands containing five- and six-membered carbocyclic rings. Such ligands, which are the sulfur analogues of the well-known croconate (<i>n</i> = 5) and rhodizonate (<i>n</i> = 6) oxocarbon ligands, function as bidentate ligands to the central Ni₂ unit. Higher energy Ni₂(CS)_<i>n</i> (<i>n</i> = 7, 6, 5) structures contain dimeric C₂S₂ ligands, which can bridge the central Ni₂ unit. Dimeric C₂S₂ ligands rather than tetrathiosquare C₄S₄ ligands are found in the lowest energy Ni₂(CS)₄ structures

DataSheet7_Role and mechanism of NCAPD3 in promoting malignant behaviors in gastric cancer.ZIP

Background:Gastric cancer (GC) is one of the major malignancies threatening human lives and health. Non-SMC condensin II complex subunit D3 (NCAPD3) plays a crucial role in the occurrence of many diseases. However, its role in GC remains unexplored.Materials and Methods:The Cancer Genome Atlas (TCGA) database, clinical samples, and cell lines were used to analyze NCAPD3 expression in GC. NCAPD3 was overexpressed and inhibited by lentiviral vectors and the CRISPR/Cas9 system, respectively. The biological functions of NCAPD3 were investigated in vitro and in vivo. Gene microarray, Gene set enrichment analysis (GSEA) and ingenuity pathway analysis (IPA) were performed to establish the potential mechanisms.Results:NCAPD3 was highly expressed in GC and was associated with a poor prognosis. NCAPD3 upregulation significantly promoted the malignant biological behaviors of gastric cancer cell, while NCAPD3 inhibition exerted a opposite effect. NCAPD3 loss can directly inhibit CCND1 and ESR1 expression to downregulate the expression of downstream targets CDK6 and IRS1 and inhibit the proliferation of gastric cancer cells. Moreover, NCAPD3 loss activates IRF7 and DDIT3 to regulate apoptosis in gastric cancer cells.Conclusion:Our study revealed that NCAPD3 silencing attenuates malignant phenotypes of GC and that it is a potential target for GC treatment.</p

DataSheet4_Role and mechanism of NCAPD3 in promoting malignant behaviors in gastric cancer.ZIP

Background:Gastric cancer (GC) is one of the major malignancies threatening human lives and health. Non-SMC condensin II complex subunit D3 (NCAPD3) plays a crucial role in the occurrence of many diseases. However, its role in GC remains unexplored.Materials and Methods:The Cancer Genome Atlas (TCGA) database, clinical samples, and cell lines were used to analyze NCAPD3 expression in GC. NCAPD3 was overexpressed and inhibited by lentiviral vectors and the CRISPR/Cas9 system, respectively. The biological functions of NCAPD3 were investigated in vitro and in vivo. Gene microarray, Gene set enrichment analysis (GSEA) and ingenuity pathway analysis (IPA) were performed to establish the potential mechanisms.Results:NCAPD3 was highly expressed in GC and was associated with a poor prognosis. NCAPD3 upregulation significantly promoted the malignant biological behaviors of gastric cancer cell, while NCAPD3 inhibition exerted a opposite effect. NCAPD3 loss can directly inhibit CCND1 and ESR1 expression to downregulate the expression of downstream targets CDK6 and IRS1 and inhibit the proliferation of gastric cancer cells. Moreover, NCAPD3 loss activates IRF7 and DDIT3 to regulate apoptosis in gastric cancer cells.Conclusion:Our study revealed that NCAPD3 silencing attenuates malignant phenotypes of GC and that it is a potential target for GC treatment.</p

DataSheet13_Role and mechanism of NCAPD3 in promoting malignant behaviors in gastric cancer.xlsx

Background:Gastric cancer (GC) is one of the major malignancies threatening human lives and health. Non-SMC condensin II complex subunit D3 (NCAPD3) plays a crucial role in the occurrence of many diseases. However, its role in GC remains unexplored.Materials and Methods:The Cancer Genome Atlas (TCGA) database, clinical samples, and cell lines were used to analyze NCAPD3 expression in GC. NCAPD3 was overexpressed and inhibited by lentiviral vectors and the CRISPR/Cas9 system, respectively. The biological functions of NCAPD3 were investigated in vitro and in vivo. Gene microarray, Gene set enrichment analysis (GSEA) and ingenuity pathway analysis (IPA) were performed to establish the potential mechanisms.Results:NCAPD3 was highly expressed in GC and was associated with a poor prognosis. NCAPD3 upregulation significantly promoted the malignant biological behaviors of gastric cancer cell, while NCAPD3 inhibition exerted a opposite effect. NCAPD3 loss can directly inhibit CCND1 and ESR1 expression to downregulate the expression of downstream targets CDK6 and IRS1 and inhibit the proliferation of gastric cancer cells. Moreover, NCAPD3 loss activates IRF7 and DDIT3 to regulate apoptosis in gastric cancer cells.Conclusion:Our study revealed that NCAPD3 silencing attenuates malignant phenotypes of GC and that it is a potential target for GC treatment.</p