Improved Insulin Resistance and Lipid Metabolism by Cinnamon Extract through Activation of Peroxisome Proliferator-Activated Receptors

Peroxisome proliferator-activated receptors (PPARs) are transcriptional factors involved in the regulation of insulin resistance and adipogenesis. Cinnamon, a widely used spice in food preparation and traditional antidiabetic remedy, is found to activate PPARγ and α, resulting in improved insulin resistance, reduced fasted glucose, FFA, LDL-c, and AST levels in high-caloric diet-induced obesity (DIO) and db/db mice in its water extract form. In vitro studies demonstrate that cinnamon increases the expression of peroxisome proliferator-activated receptors γ and α (PPARγ/α) and their target genes such as LPL, CD36, GLUT4, and ACO in 3T3-L1 adipocyte. The transactivities of both full length and ligand-binding domain (LBD) of PPARγ and PPARα are activated by cinnamon as evidenced by reporter gene assays. These data suggest that cinnamon in its water extract form can act as a dual activator of PPARγ and α, and may be an alternative to PPARγ activator in managing obesity-related diabetes and hyperlipidemia

Parameter identification of BIPT system using chaotic-enhanced fruit fly optimization algorithm

Bidirectional inductive power transfer (BIPT) system facilitates contactless power transfer between two sides and across an air-gap, through weak magnetic coupling. Typically, this system is nonlinear high order system which includes nonlinear switch components and resonant networks, developing of accurate model is a challenging task. In this paper, a novel technique for parameter identification of a BIPT system is presented by using chaotic-enhanced fruit fly optimization algorithm (CFOA). The fruit fly optimization algorithm (FOA) is a new meta-heuristic technique based on the swarm behavior of the fruit fly. This paper proposes a novel CFOA, which employs chaotic sequence to enhance the global optimization capacity of original FOA. The parameter identification of the BIPT system is formalized as a multi-dimensional optimization problem, and an objective function is established minimizing the errors between the estimated and measured values. All the 11 parameters of this system (Lpi, LT, Lsi, Lso, CT, Cs, M, Rpi, RT, Rsi and Rso) can be identified simultaneously using measured input–output data. Simulations show that the proposed parameter identification technique is robust to measurements noise and variation of operation condition and thus it is suitable for practical application

FGBERT: Function-Driven Pre-trained Gene Language Model for Metagenomics

Metagenomic data, comprising mixed multi-species genomes, are prevalent in diverse environments like oceans and soils, significantly impacting human health and ecological functions. However, current research relies on K-mer representations, limiting the capture of structurally relevant gene contexts. To address these limitations and further our understanding of complex relationships between metagenomic sequences and their functions, we introduce a protein-based gene representation as a context-aware and structure-relevant tokenizer. Our approach includes Masked Gene Modeling (MGM) for gene group-level pre-training, providing insights into inter-gene contextual information, and Triple Enhanced Metagenomic Contrastive Learning (TEM-CL) for gene-level pre-training to model gene sequence-function relationships. MGM and TEM-CL constitute our novel metagenomic language model {\NAME}, pre-trained on 100 million metagenomic sequences. We demonstrate the superiority of our proposed {\NAME} on eight datasets

trans-N,N,N′,N′-Tetra­kis(carboxy­meth­yl)cyclo­hexane-1,2-diammonium tetra­chloridocadmium(II) tetra­hydrate

In the title compound, (C14H24N2O8)[CdCl4]·4H2O, the Cd atom in the tetra­hedral [CdCl4]2− anion lies on a twofold rotation axis, and the diprotonated organic mol­ecule, trans-N,N,N′,N′-tetra­kis(carb­oxy­meth­yl)cyclo­hexane-1,2-diammon­ium, has 2 symmetry with the twofold rotation axis running through the mid-point of two C—C bonds in the cyclo­hexane unit. In the crystal structure, classical intra­molecular O—H⋯O and N—H⋯O and inter­molecular O—H⋯O, N—H⋯O, O—H⋯Cl and C—H⋯Cl hydrogen bonds are observed

{1,8-Bis[2-(2-oxidobenzyl­idene­amino)phen­oxy]-3,6-dioxaocta­ne}nitrato­praseodymium(III) trichloro­methane solvate

In the title compound, [Pr(C32H30N2O6)(NO3)]·CHCl3, the PrIII ion is ten-coordinated by eight O atoms and two N atoms from the acyclic crown-type Schiff base ligand and the bidentate nitrate group. The coordination polyhedron around PrIII is a distorted bicapped square anti­prism. The chloro­form solvent mol­ecule is not involved either in coordination to the PrIII center or in hydrogen bonding to the complex. The Pr—O(phenolate) bonds are significantly shorter than the Pr—O(ether) and Pr—O(nitrate) bonds, which suggests that the Pr—O(phenolate) bond is stronger than these other bonds. In the crystal structure, the acyclic crown-type Schiff base ligand wraps around the PrIII centre, forming a pseudo-ring

The negative interplay between Aurora A/B and BRCA1/2 controls cancer cell growth and tumorigenesis via distinct regulation of cell cycle progression, cytokinesis, and tetraploidy

It is well known that the activation of Aurora A/B (Aur A/B) or inactivation of BRCA1/2 induces tumor formation. Others and we have reported that the mutual suppression between Aur A/B and BRCA1/2 may manipulate cancer cell growth and tumorigenesis, however, the interactive regulation and mechanism between these molecules are still elusive. In this study, by consecutive silencing of Aur A/B or/and BRCA1/2 with specific shRNAs, we showed that, in BRCA2-deficient pancreatic cancer cell line Capan-1 and in ovarian cancer cell line OVCA433, Aur A/B and BRCA1/2 inversely regulated the expression of each other likely through proteasome-mediated proteolysis but not through gene transcription. Aur A/B and BRCA1/2 conversely regulated cell cycle progression mainly through control of p53 and cyclin A. Moreover, the disruption of Aur A/B blocked abnormal cytokinesis and decreased cell multinuclearity and chromosome tetraploidy, whereas the deprivation of BRCA1/2 promoted the abnormal cytokinesis and enhanced the cell multinuclearity and tetraploidy. Furthermore, we showed by animal assays that the depletion of Aur A/B inhibited tumor growth of both cell lines, while the knockdown of BRCA1/2 promoted the tumor growth. However, the concurrent silencing of Aur A/B and BRCA1/2 diminished the effects of these molecules on the regulation of cell cycle, cytokinesis, and tetraploidy, leading to the burdened tumor sizes similar to those induced by scrambled shRNA-treated control cells. In summary, our study revealed that the negative interplay between Aur A/B and BRCA1/2 inversely controls the cell proliferation, cell cycle progression, cell multinuclearity, and tetraploidization to modulate tumorigenesis