Spin Crossover in [Fe(qsal-5-Br)] Complexes with a Quinoline-Substituted Qsal Ligand.

Using a quinoline substituted Qsal ligand, Hqsal-5-Br (Hqsal-5-Br = N-(5-bromo-8-quinolyl)salicylaldimine), four Fe complexes, [Fe(qsal-5-Br)]A·CHOH (Y = NO (), BF (), PF (), OTf (), were prepared and characterized. Structure analysis revealed that complex contained two species ((̅) and ()). In these compounds except , the [Fe(qsal-5-Br)] cations form 1D chains through π-π interactions and other weak interactions.

Two new alkaloids from the endophytic fungus sp. HM230 isolated from Maxim.

Endophytic fungi is an important source for the discovery of bioactive natural compounds. A chemical investigation of the ethyl acetate extract of the endophytic fungus sp. HM230 derived from stems of the herb Maxim led to isolation of five alkaloids, including two new compounds, schizophyllins M () and N (), along with three known ones (-).

Modulating the Structures and Magnetic Properties of Dy(III) Single-Molecule Magnets through Acid-Base Regulation.

Chemical modulation on the structures and physical properties of the coordination complexes is of great interest for the preparation of new functional materials. By changing the acidity or basicity of the reaction medium, the deprotonation degree of a multidentate ligand with multiple active protons, Hdaps (Hdaps = ','″-((1,1')-pyridine-2,6-diylbis(ethan-1-yl-1-ylidene))bis(2-hydroxybenzohydrazide)), can be regulated on purpose. With this ligand of different deprotonation and charges, three new Dy complexes ([Dy(Hdaps)(CHCOO)(EtOH)]·CHCOOH (), [Dy(Hdaps)(EtOH)(HO)(MeOH)](CFSO)·(HO) (), and [Dy(Hdaps)(Hdaps)(μ-OH)(EtOH)(HO)] ()) of different nuclearities (mono-, di-, and trinuclear for to , respectively) have been synthesized and characterized structurally and magnetically.

microRNA-19a protects osteoblasts from dexamethasone via targeting TSC1.

Activation of mTOR complex 1 (mTORC1) could protect human osteoblasts from dexamethasone. Tuberous sclerosis complex 1 (TSC1) is mTORC1 upstream inhibitory protein. We demonstrate here that microRNA-19a ("miR-19a", -3p) targets the 3' untranslated regions of .

Activation of Nrf2 by MIND4-17 protects osteoblasts from hydrogen peroxide-induced oxidative stress.

MIND4-17 is a recently developed NF-E2-related factor 2 (Nrf2) activator, which uniquely causes Nrf2 disassociation from Keap1. Here, we showed that pretreatment with MIND4-17 significantly inhibited hydrogen peroxide (HO)-induced viability reduction of primary osteoblasts and OB-6 osteoblastic cells. Meanwhile, MIND4-17 inhibited both apoptotic and non-apoptotic osteoblast cell death by HO.

MicroRNA-200a activates Nrf2 signaling to protect osteoblasts from dexamethasone.

Treatment with dexamethasone in human osteoblasts leads to oxidative stress and cell injures. NF-E2-related factor 2 (Nrf2) is a key anti-oxidant signaling. We want to induce Nrf2 activation via microRNA-mediated silencing its suppressor Keap1.

Activation of AMP-activated protein kinase by compound 991 protects osteoblasts from dexamethasone.

Dexamethasone (Dex) induces direct cytotoxicity to cultured osteoblasts. The benzimidazole derivative compound 991 ("C991") is a novel and highly-efficient AMP-activated protein kinase (AMPK) activator. Here, in both MC3T3-E1 osteoblastic cells and primary murine osteoblasts, treatment with C991 activated AMPK signaling, and significantly attenuated Dex-induced apoptotic and non-apoptotic cell death.

Vitamin D deficiency causes insulin resistance by provoking oxidative stress in hepatocytes.

Vitamin D deficiency could cause insulin resistance. However, the underlying mechanisms are unclear. The 1α-Hydroxylase ["1α(OH)ase"] is a key enzyme for activate vitamin D3 synthesis.

Insulin resistance in vitamin D-deficient mice is alleviated by n-acetylcysteine.

Vitamin D deficiency will lead to insulin resistance. In the current study, vitamin D3 1α-Hydroxylase ["1α(OH)ase"] knockout mice were generated to mimic vitamin D deficiency . As compared to the wild-type mice, the liver tissues of the knockout mice showed impaired insulin signaling, decreased glucose transporter 4 expression and increased reactive oxygen species production.

Assessment of GSK1904529A as a promising anti-osteosarcoma agent.

The insulin growth factor-I receptor (IGF1R) signaling is a key mechanism for osteosarcoma (OS) cell proliferation. GSK1904529A is a novel small molecule IGF1R kinase inhibitor. Its activity against OS cells was tested.

Identification of Key Gene Modules in Human Osteosarcoma by Co-Expression Analysis Weighted Gene Co-Expression Network Analysis (WGCNA).

Osteosarcoma is the eighth-most common form of childhood cancer, comprising about 20% of all primary bone cancers. To date, systemic co-expression analysis for this cancer is still insufficient to explain the pathogenesis of poorly understood OC. The objective of this study was to construct a gene co-expression network to predict clusters of candidate genes involved in the pathogenesis of osteosarcoma.

B7-H3 protein expression in a murine model of osteosarcoma.

Osteosarcoma is an aggressive type of bone tumor that commonly occurs in pediatric age groups. The complete molecular mechanisms behind osteosarcoma formation and progression require elucidation. B7-H3 is a protein of the B7 family that acts as a co-stimulatory molecule with a significant role in adaptive immune responses.

[Establishment of Human Acute B-Lymphoblastic Leukemia--NOD/SCID Xenotransplant Mouse Model].

Objective: To establish human B-acute lymphoblastic leukemia NOD/SCID mouse model.

Methods: The unirradiated mice aged 4-5 weeks were injected with Nalm-6 cells via the tail vein. Successful transplantation was assessed by the general state, bone marrow smear and histopathologic examination.

Assimilative branches and leaves of the desert plant Alhagi sparsifolia Shap. possesses a different adaptation mechanism to shade.

Leaves and assimilative branches are crucial to the life cycle of Alhagi sparsifolia Shap. (Fabaceae), which grows in high-irradiance environments and is the main vegetation in the forelands of the Taklamakan Desert. This plant has an important role in wind protection and sand fixation at the oasis-desert transition zone.

Activation of astrocytes in the anterior cingulate cortex contributes to the affective component of pain in an inflammatory pain model.

The anterior cingulate cortex (ACC) has been implicated as a key structure in the affective component of pain (such as unpleasantness or aversion). Recent evidence suggests that activation of spinal astrocytes contributes to the development and maintenance of the sensory component of pain after peripheral inflammation. However, whether the astrocytes in the ACC contribute to the affective component of pain is unknown.