1-[6-(9H-Carbazol-9-yl)hex­yl]-2-phenyl-1H-benzimidazole

The mol­ecule of the title compound, C31H29N3, contains a hexyl chain, a coordination unit (benzimidazole) and a functional group (carbazole). The benzimidazole ring is not coplanar with either the phenyl ring or the carbazole system, making dihedral angles of 43.26 (3) and 39.03 (2)°, respectively. The dihedral angle between the phenyl ring and the carbazole system is 24.42 (3)°. The hexyl Cβ atom (with respect to benzimidazole) deviates by 1.124 (2) Å from the benzimidazole plane, although the Cα atom lies in the plane. The hexyl Cβ atom (with respect to carbazole) deviates by 1.315 (1) Å from the carbazole plane, although the Cα atom lies in the plane. The crystal structure is stabilized by inter­molecular C—H⋯π inter­actions

Generation of Oligodendrocyte Progenitor Cells From Mouse Bone Marrow Cells.

Oligodendrocyte progenitor cells (OPCs) are a subtype of glial cells responsible for myelin regeneration. Oligodendrocytes (OLGs) originate from OPCs and are the myelinating cells in the central nervous system (CNS). OLGs play an important role in the context of lesions in which myelin loss occurs. Even though many protocols for isolating OPCs have been published, their cellular yield remains a limit for clinical application. The protocol proposed here is novel and has practical value; in fact, OPCs can be generated from a source of autologous cells without gene manipulation. Our method represents a rapid, and high-efficiency differentiation protocol for generating mouse OLGs from bone marrow-derived cells using growth-factor defined media. With this protocol, it is possible to obtain mature OLGs in 7-8 weeks. Within 2-3 weeks from bone marrow (BM) isolation, after neurospheres formed, the cells differentiate into Nestin+ Sox2+ neural stem cells (NSCs), around 30 days. OPCs specific markers start to be expressed around day 38, followed by RIP+O4+ around day 42. CNPase+ mature OLGs are finally obtained around 7-8 weeks. Further, bone marrow-derived OPCs exhibited therapeutic effect in shiverer (Shi) mice, promoting myelin regeneration and reducing the tremor. Here, we propose a method by which OLGs can be generated starting from BM cells and have similar abilities to subventricular zone (SVZ)-derived cells. This protocol significantly decreases the timing and costs of the OLGs differentiation within 2 months of culture

3D Stretchable Arch Ribbon Array Fabricated via Grayscale Lithography.

Microstructures with flexible and stretchable properties display tremendous potential applications including integrated systems, wearable devices and bio-sensor electronics. Hence, it is essential to develop an effective method for fabricating curvilinear and flexural microstructures. Despite significant advances in 2D stretchable inorganic structures, large scale fabrication of unique 3D microstructures at a low cost remains challenging. Here, we demonstrate that the 3D microstructures can be achieved by grayscale lithography to produce a curved photoresist (PR) template, where the PR acts as sacrificial layer to form wavelike arched structures. Using plasma-enhanced chemical vapor deposition (PECVD) process at low temperature, the curved PR topography can be transferred to the silicon dioxide layer. Subsequently, plasma etching can be used to fabricate the arched stripe arrays. The wavelike silicon dioxide arch microstructure exhibits Young modulus and fracture strength of 52 GPa and 300 MPa, respectively. The model of stress distribution inside the microstructure was also established, which compares well with the experimental results. This approach of fabricating a wavelike arch structure may become a promising route to produce a variety of stretchable sensors, actuators and circuits, thus providing unique opportunities for emerging classes of robust 3D integrated systems

Antitumor efficacy of combination of interferon-gamma-inducible protein 10 gene with gemcitabine, a study in murine model

<p>Abstract</p> <p>Background</p> <p>Interferon-γ-inducible protein 10 (IP-10) is a potent inhibitor of tumor angiogenesis. It has been reported that the antiangiogenic therapy combined with chemotherapy has synergistic effects.</p> <p>Methods</p> <p>To elucidate the mechanisms of IP-10 gene combined with a chemotherapy agent, we intramuscularly injected pBLAST-IP-10 expression plasmid combined with gemcitabine into tumor-bearing mice.</p> <p>Results</p> <p>The proliferation of endothelial cells was effectively inhibited by IP-10 combined with gemcitabine <it>in vitro</it>. Treatment with pBLAST-IP-10 twice a week for 4 weeks combined with gemcitabine 10 mg/kg (once a week) resulted in sustained high level of IP-10 protein in serum, inhibition of tumor growth and prolongation of the survival of tumor-bearing mice. Compared with administration of IP-10 plasmid or gemcitabine alone, the angiogenesis in tumors were apparently inhibited, and the numbers of apoptotic cells and lymphocytes in tumor increased in the combination therapy group.</p> <p>Conclusion</p> <p>Our data indicate that the gene therapy of antiangiogenesis by intramuscular delivery of plasmid DNA encoding IP-10 combined with gemcitabine has synergistic effects on tomor by inhibiting the proliferation of endothelail cells, inducing the apoptosis of tumor cells, and recruiting lymphocytes to tumor in murine models. The present findings provided evidence of antitumor effects of genetherapy combined with chemotherapy.</p

Inhibitory Effects of Baicalin on the Expression and Activity of CYP3A Induce the Pharmacokinetic Changes of Midazolam in Rats

Baicalin, a flavonoid compound isolated from Scutellaria baicalensis, has been shown to possess antiinflammatory, antiviral, antitumour, and immune regulatory properties. The present study evaluated the potential herb-drug interaction between baicalin and midazolam in rats. Coadministration of a single dose of baicalin (0.225, 0.45, and 0.90 g/kg, i.v.) with midazolam (10 mg/kg, i.v.) in rats resulted in a dose-dependent decrease in clearance (CL) from 25%  (P<0.05) to 34%  (P<0.001) with an increase in AUC0−∞ from 47%  (P<0.05) to 53%  (P<0.01). Pretreatment of baicalin (0.90 g/kg, i.v., once daily for 7 days) also reduced midazolam CL by 43%  (P<0.001), with an increase in AUC0−∞ by 87%  (P<0.01). Multiple doses of baicalin decreased the expression of hepatic CYP3A2 by approximately 58%  (P<0.01) and reduced midazolam 1′-hydroxylation by 23%  (P<0.001) and 4′-hydroxylation by 21%  (P<0.01) in the liver. In addition, baicalin competitively inhibited midazolam metabolism in rat liver microsomes in a concentration-dependent manner. Our data demonstrated that baicalin induced changes in the pharmacokinetics of midazolam in rats, which might be due to its inhibition of the hydroxylation activity and expression of CYP3A in the liver