Quantifying weak interactions in ferroelectric and paraelectric phases of phenazine and chloroanilic acid co-crystal using experimental and theoretical electron densities.

The co-crystal of phenazine and chloroanilic acid is known to display paraelectric properties at room temperature. It shows a paraelectric to ferroelectric phase transition at 253 K and has an incommensurately modulated ferroelectric phase below 137 K. High-resolution synchrotron X-ray data were collected at 160 K to model the experimental electron-density distributions, and derived topological properties from the electron density were used to quantify the weak interactions responsible for the origin of the ferroelectric phase. The structure and non-covalent interactions are analysed using Hirshfeld surfaces and energy frameworks. The topological properties, energies, atomic charges and molecular electrostatic potential surfaces are determined from the experimental data, further supported by theoretical calculations. The results from the ferroelectric phase are compared with the paraelectric phase. Although the structural descriptions indicate neutral phenazine and chloroanilic acid molecules in the ferroelectric phase, the topological properties of the electron density indicate a considerable amount of proton transfer in the O-H...O hydrogen bond. Indeed, the displaced H atom in the O-H...O hydrogen bond suggests a mixed covalent/polar nature of chemical bonding. Subtle changes in the chemical bonding and proton-transfer pathways could be detected from the high-resolution electron-density studies.

Design of Resources Allocation in 6G Cybertwin Technology Using the Fuzzy Neuro Model in Healthcare Systems.

In 6G edge communication networks, the machine learning models play a major role in enabling intelligent decision-making in case of optimal resource allocation in case of the healthcare system. However, it causes a bottleneck, in the form of sophisticated memory calculations, between the hidden layers and the cost of communication between the edge devices/edge nodes and the cloud centres, while transmitting the data from the healthcare management system to the cloud centre via edge nodes. In order to reduce these hurdles, it is important to share workloads to further eliminate the problems related to complicated memory calculations and transmission costs. The effort aims mainly to reduce storage costs and cloud computing associated with neural networks as the complexity of the computations increases with increasing numbers of hidden layers. This study modifies federated teaching to function with distributed assignment resource settings as a distributed deep learning model. It improves the capacity to learn from the data and assigns an ideal workload depending on the limited available resources, slow network connection, and more edge devices. Current network status can be sent to the cloud centre by the edge devices and edge nodes autonomously using cybertwin, meaning that local data are often updated to calculate global data. The simulation shows how effective resource management and allocation is better than standard approaches. It is seen from the results that the proposed method achieves higher resource utilization and success rate than existing methods. Index Terms are fuzzy, healthcare, bioinformatics, 6G wireless communication, cybertwin, machine learning, neural network, and edge.

Crystal structure, DFT and Hirshfeld surface analysis of (E)-N'-[(1-chloro-3,4-di-hydro-naph-thal-en-2-yl)methyl-idene]benzohydrazide monohydrate.

In the title compound, C18H15ClN2O·H2O, a benzohydrazide derivative, the dihedral angle between the mean plane of the di-hydro-naphthalene ring system and the phenyl ring is 17.1 (2)°. In the crystal, O-H⋯O, N-H⋯O and C-H⋯O hydrogen bonds link the benzohydrazide and water mol-ecules, forming a layer parallel to the bc plane. Hirshfeld surface analysis and two-dimensional fingerprint plots indicate that the most important contributions to the crystal packing are from H⋯H (45.7%) and H⋯C/C⋯H (20.2%) contacts.

A click chemistry approach for the synthesis of cyclic ureido tethered coumarinyl and 1-aza coumarinyl 1,2,3-triazoles as inhibitors of Mycobacterium tuberculosis H37Rv and their in silico studies.

Nucleoside bases like uracil, pharmacophoric triazoles and benzimidazolones have been used during the present study to design molecular matrices for antitubercular activity, employing Click Chemistry. Click triazoles 4/7/10 have been obtained by the reaction of 4-(Azidomethyl)-2H-chromen-2-ones/quinolin-2(1H)-ones 3 and propargyl ethers 2/6/9 derived from theophylline/6-methyl uracil/2-benzimidazolone respectively. In addition to spectral data structures have been confirmed by single crystal X-ray diffraction studies in case of uracil bis alkyne (6) and theophylline mono triazole (4c). Theophylline linked mono triazoles, 4(a-d) and 6-methyl uracil linked bis triazoles, 7(a-e) have been found to inhibit Mycobacterium tuberculosis H37Rv with MIC values in the range 55.62-115.62 µM. Benzimidazolone bis triazoles, 10(a-n) showed better activity with MIC in the range 2.33-18.34 µM. Molecular modeling studies using Surflex-Dock algorithm supported our results.

Crystal structure of 4-(4b,8a-di-hydro-9H-pyrido[3,4-b]indol-1-yl)-7-methyl-2H-chromen-2-one.

The title compound, C21H14N2O2, was prepared by Pictet-Spengler cyclization of tryptamine and 4-formyl coumarin. In the mol-ecule, the dihedral angle between the mean planes of the coumarin and ß-carboline ring systems is 63.8 (2)°. In the crystal, mol-ecules are linked via N-H⋯N hydrogen bonds, forming chains along the b-axis direction. Within the chains, there are a number of offset π-π inter-actions present [shortest inter-centroid distance = 3.457 (2) Å].

The crystal structure of 6-(4-chloro-phen-yl)-2-(4-methyl-benz-yl)imidazo[2,1-b][1,3,4]thia-diazole-5-carbaldehyde.

In the title imidazo[2,1-b][1,3,4]thia-diazole derivative, C19H14ClN3OS, the 4-methyl-benzyl and chloro-phenyl rings are inclined to the planar imidazo[2,1-b][1,3,4]thia-diazole moiety (r.m.s. deviation = 0.012 Å) by 64.5 (1) and 3.7 (1)°, respectively. The mol-ecular structure is primarily stabilized by a strong intra-molecular C-H⋯O hydrogen bond, leading to the formation of a pseudo-seven-membered S(7) ring motif, and a short intra-molecular C-H⋯N contact forming an S(5) ring motif. In the crystal, mol-ecules are linked by pairs of C-H⋯S hydrogen bonds, forming inversion dimers. The dimers are linked by C-H⋯O and C-H⋯π inter-actions, forming chains propagating along [110].

Superdeformed and Triaxial States in

Shape parameters of a weakly deformed ground-state band and highly deformed slightly triaxial sideband in ^{42}Ca were determined from E2 matrix elements measured in the first low-energy Coulomb excitation experiment performed with AGATA. The picture of two coexisting structures is well reproduced by new state-of-the-art large-scale shell model and beyond-mean-field calculations. Experimental evidence for superdeformation of the band built on 0_{2}^{+} has been obtained and the role of triaxiality in the A∼40 mass region is discussed. Furthermore, the potential of Coulomb excitation as a tool to study superdeformation has been demonstrated for the first time.

NPC1L1 knockout protects against colitis-associated tumorigenesis in mice.

BACKGROUND: Colorectal cancer is strongly associated with lipid metabolism. NPC1L1, a sterol transporter, plays a key role in modulating lipid homeostasis in vivo. Its inhibitor, ezetimibe, began to be used clinically to lower cholesterol and this caused the great debate on its role in causing carcinogenesis. Here we explored the role of NPC1L1 in colorectal tumorigenesis. METHODS: Wild-type mice and NPC1L1(-/-) (NPC1L1 knockout) mice were treated with azoxymethane (AOM)-dextran sodium sulfate (DSS) to induce colitis-associated colorectal tumorigenesis. Mice were sacrificed 10, 15, 18 or 20 weeks after AOM treatment, respectively. Colorectal tumors were counted and analyzed. Plasma lipid concentrations were measured using enzymatic reagent kit. Protein expression level was assayed by western blot. RESULTS: NPC1L1(-/-) mice significantly had fewer tumors than wild-type. The ratio of malignant/tumor in NPC1L1(-/-) mice was significantly lower than in wild-type 20 weeks after AOM-DSS treatment. NPC1L1 was highly expressed in the small intestine of wild-type mice but its expression was undetectable in colorectal mucous membranes or tumors in either group. NPC1L1 knockout decreased plasma total cholesterol and phospholipid. NPC1L1(-/-) mice had significant lower intestinal inflammation scores and expressed inflammatory markers p-c-Jun, p-ERK and Caspase-1 p20 lower than wild-type. NPC1L1 knockout also reduced lymphadenectasis what may be caused by inflammation. NPC1L1 knockout in mice decreased ß-catenin in tumors and regulated TGF-ß and p-gp in adjacent colons or tumors. There was not detectable change of p53 by NPC1L1 knockout. CONCLUSIONS: Our results provide the first evidence that NPC1L1 knockout protects against colitis-associated tumorigenesis. NPC1L1 knockout decreasing plasma lipid, especially cholesterol, to reduce inflammation and decreasing ß-catenin, p-c-Jun and p-ERK may be involved in the mechanism.

Crystal structure of 6,6'-dimethyl-2H,2'H-3,4'-bichromene-2,2'-dione.

In the title compound, C20H14O4, the dihedral angle between the two coumarin ring systems is 52.37 (19)°, showing a gauche arrangement across the C-C bond which links the two units. The carbonyl groups of the two coumarin units adopt an s-trans arrangement. In the crystal, pairs of C-H⋯O hydrogen bonds and π-π inter-actions [centroid-centroid distance = 3.631 (2) Å] connect the mol-ecules into inversion dimers.

Crystal structure of 3-({[(morpholin-4-yl)carbono-thio-yl]sulfan-yl}acet-yl)phenyl benzoate.

In the title compound, C20H19NO4S2, the morpholine ring adopts the expected chair conformation. The central phenyl ring makes dihedral angles of 67.97 (4) and 7.74 (3)°, respectively, with the benzoate phenyl ring and the morpholine mean plane. In the crystal, mol-ecules are linked by C-H⋯O hydrogen bonds, forming zigzag chains along the b-axis direction. C-H⋯π inter-actions link centrosymmetrically related mol-ecules, reinforcing the three-dimensional structure.

Crystal structure of 3-[(E)-2-(4-phenyl-1,3-thia-zol-2-yl)hydrazin-1-yl-idene]indolin-2-one.

In the title mol-ecule, C17H12N4OS, the thia-zole ring forms a dihedral angle of 10.8 (2)° with the phenyl ring and an angle of 3.1 (3)° with the indole ring system [which has a maximum deviation of 0.035 (2) Å]. The dihedral angle between the planes of the phenyl ring and the indole ring system is 11.5 (1)°. An intra-molecular N-H⋯O hydrogen bond is observed. In the crystal, pairs of N-H⋯O hydrogen bonds form inversion dimers with an R (2) 2(8) graph-set motif.

4-{[Bis(2-hy-droxy-eth-yl)amino]-meth-yl}-6-meth-oxy-2H-chromen-2-one.

In the title compound, C(15)H(19)NO(5), an intra-molecular O-H⋯O hydrogen bond links the hy-droxy-ethyl side chains, forming a seven-membered ring. In the crystal, mol-ecules are linked into chains via O-H⋯O hydrogen bonds along the b axis. Further, mol-ecules are linked by weak inter-molecular C-H⋯O and π-π stacking inter-actions [centroid-centroid distance = 3.707 (4) Å].

Dietary conjugated linoleic Acid and hepatic steatosis: species-specific effects on liver and adipose lipid metabolism and gene expression.

Objective. To summarize the recent studies on effect of conjugated linoleic acid (CLA) on hepatic steatosis and hepatic and adipose lipid metabolism highlighting the potential regulatory mechanisms. Methods. Sixty-four published experiments were summarized in which trans-10, cis-12 CLA was fed either alone or in combination with other CLA isomers to mice, rats, hamsters, and humans were compared. Summary and Conclusions. Dietary trans-10, cis-12 CLA induces a severe hepatic steatosis in mice with a more muted response in other species. Regardless of species, when hepatic steatosis was present, a concurrent decrease in body adiposity was observed, suggesting that hepatic lipid accumulation is a result of uptake of mobilized fatty acids (FA) from adipose tissue and the liver's inability to sufficiently increase FA oxidation and export of synthesized triglycerides. The potential role of liver FA composition, insulin secretion and sensitivity, adipokine, and inflammatory responses are discussed as potential mechanisms behind CLA-induced hepatic steatosis.