25 research outputs found
Additional file 1: Figure S1. of Carbon Nanotube-Silicon Nanowire Heterojunction Solar Cells with Gas-Dependent Photovoltaic Performances and Their Application in Self-Powered NO2 Detecting
Depth-resolved Auger spectra of silicon and oxygen atomic concentrations in a fresh Si substrate and after 1000Ă‚Â ppm NO2 oxidation. (TIF 7878Ă‚Â kb
Controlled Rod Nanostructured Assembly of Diphenylalanine and Their Optical Waveguide Properties
Diphenylalanine (FF) microrods were obtained by manipulating the fabrication conditions. Fourier transform infrared (FTIR), circular dichroism (CD), fluorescence (FL) spectroscopy, and X-ray diffraction (XRD) measurements revealed the molecular arrangement within the FF microrods, demonstrating similar secondary structure and molecular arrangement within FF microtubes and nanofibers. Accordingly, a possible mechanism was proposed, which may provide important guidance on the design and assembly manipulation of peptides and other biomolecules. Furthermore, characterization of a single FF microrod indicates that the FF microrod can act as an active optical waveguide material, allowing locally excited photoluminescence to propagate along the length of the microrod with coupling out at the microrod tips
Transporting a Tube in a Tube
LbL-assembled
tubes were employed for micro/nanoscale cargo transportation
through the kinesin-microtubule system. Selectively modified with
kinesins onto the inner tube walls through Ni–NTA complexes,
these tubes can work as channels for microtubules. A motility assay
shows the smooth movement of microtubules along the tube inner wall
powered by the inside immobilized kinesins. It could be envisioned
that cargoes with different sizes can be transported through these
tubular channels with little outside interruption
Complex Assembly of Polymer Conjugated Mesoporous Silica Nanoparticles for Intracellular pH-Responsive Drug Delivery
There is a great challenge in constructing
pH-responsive drug delivery
systems in biomedical application research. Many nanocomposites are
intended to be pH-responsive as drug carriers because of a tumorous
or intracellular mildly acidic environment. However, it is always
difficult to find an appropriate system for quick response and release
before the carrier is excreted from the living system. In this work,
hyperbranched polymer, hyperbranched polyglycerol (hPG), and conjugated
mesoporous silica nanoparticles (MSNs) were assembled as complexes
to serve as drug carriers. Herein, the conjugated polymer-MSNs interacted
through the Schiff base bond, which possessed a mildly acidic responsive
property. Interestingly, the assembled system could rapidly respond
and release guest molecules inside cancer cells. This would make the
entrapped drug released before the carriers escape from the endosome
counterpart. The results show that the assembled composite complexes
can be considered to be a drug delivery system for cancer therapy
Assembled Hemoglobin and Catalase Nanotubes for the Treatment of Oxidative Stress
Hemoglobin-based
nanotubes for the treatment of oxidative stress
are successfully fabricated via covalent layer-by-layer assembly.
Catalase, the most efficient enzyme for scavenging the hydrogen peroxide
(H<sub>2</sub>O<sub>2</sub>), is embedded into the inner pores of
the hemoglobin/dialdehyde heparin (Hb/DHP)<sub>5</sub> nanotubes via
covalent bonding to protect the delicate enzyme from inactivation
after the removal of the polycarbonate (PC) template. Dialdehyde heparin
(DHP) as wall components is a cross-linker. The biocompatibility and
capabilities of the nanotubes to protect the cells under oxidative
stress are characterized with the Cell Counting Kit-8 (CCK-8). The
scavenging capabilities of four kinds of autofluorescent nanotubes
are tested through the reaction with H<sub>2</sub>O<sub>2</sub> by
the measurement of the UV–vis absorbance at 240 nm. All the
experimental results show that the assembled hemoglobin-based nanotubes
possess H<sub>2</sub>O<sub>2</sub>-scavenging capacity as well as
biocompatibility, indicating the potential application in the treatment
of oxidative stress
Modulated Expression of Genes Encoding Estrogen Metabolizing Enzymes by G1-Phase Cyclin-Dependent Kinases 6 and 4 in Human Breast Cancer Cells
<div><p>G1-phase cell cycle defects, such as alterations in cyclin D1 or cyclin-dependent kinase (cdk) levels, are seen in most tumors. For example, increased cyclin D1 and decreased cdk6 levels are seen in many human breast tumors. Overexpression of cdk6 in breast tumor cells in culture has been shown to suppress proliferation, unlike the growth stimulating effects of its close homolog, cdk4. In addition to directly affecting proliferation, alterations in cdk6 or cdk4 levels in breast tumor cells also differentially influence levels of numerous steroid metabolic enzymes (SMEs), including those involved in estrogen metabolism. Overexpression of cdk6 in tumor cell lines having low cdk6 resulted in decreased levels of mRNAs encoding aldo-keto reductase (AKR)1C1, AKR1C2 and AKR1C3, which are hydroxysteroid dehydrogenases (HSDs) involved in steroid hormone metabolism. In contrast, increasing cdk4 dramatically increased these transcript levels, especially those encoding AKR1C3, an enzyme that converts estrone to 17β-estradiol, a change that could result in a pro-estrogenic state favoring tumor growth. Effects on other estrogen metabolizing enzymes, including cytochrome P450 (CYP) 19 aromatase, 17β-HSD2, and CYP1B1 transcripts, were also observed. Interactions of cdk6 and cdk4, but not cyclin D1, with the promoter region of a cdk-regulated gene, 17β-HSD2, were detected. The results uncover a previously unsuspected link between the cell cycle and hormone metabolism and differential roles for cdk6 and cdk4 in a novel mechanism for pre-receptor control of steroid hormone action, with important implications for the origin and treatment of steroid hormone-dependent cancers.</p></div
Complex Assembly of Polymer Conjugated Mesoporous Silica Nanoparticles for Intracellular pH-Responsive Drug Delivery
There is a great challenge in constructing
pH-responsive drug delivery
systems in biomedical application research. Many nanocomposites are
intended to be pH-responsive as drug carriers because of a tumorous
or intracellular mildly acidic environment. However, it is always
difficult to find an appropriate system for quick response and release
before the carrier is excreted from the living system. In this work,
hyperbranched polymer, hyperbranched polyglycerol (hPG), and conjugated
mesoporous silica nanoparticles (MSNs) were assembled as complexes
to serve as drug carriers. Herein, the conjugated polymer-MSNs interacted
through the Schiff base bond, which possessed a mildly acidic responsive
property. Interestingly, the assembled system could rapidly respond
and release guest molecules inside cancer cells. This would make the
entrapped drug released before the carriers escape from the endosome
counterpart. The results show that the assembled composite complexes
can be considered to be a drug delivery system for cancer therapy
Immunohistochemical detection of cdk6, cdk4, and AKR1C3 in MDA-MB-468 cell lines transfected to express increased levels of cdk6 or cdk4.
<p>In the top row of panel (<b>A</b>), cdk6 was detected by immunohistochemistry (cdk6 IHC) in parental MDA-MB-468 cells and in cell lines transfected to express increased levels of either cdk6 (“468-cdk6” cells) or cdk4 (“468-cdk4” cells). In the second row, the 3 cell types were assessed for cdk4 levels. In the top row of panel (<b>B</b>), cells expressing increased amounts of cdk6 (“468-cdk6” cells) were analyzed by IHC for cdk6, cdk4, or AKR1C3. In the second row, cells expressing increased amounts of cdk4 (“468-cdk4” cells) were analyzed for the 3 molecules by IHC. Magnification: x200. The results indicate that nearly all of the cdk4-transfected cells have greatly increased levels of AKR1C3 protein.</p
Regulatory functions of cdk6 and cdk4 in breast tumor epithelial cells: interactions of the cell cycle and steroid hormone metabolism and function.
<p>Cdk4 and cdk6 interact with cyclin D1 to regulate cell cycle progression and proliferation, through Rb and E2F-family proteins. The cdks can also regulate levels of SMEs, including the AKR1C-family of enzymes. Induction or suppression of AKR1C-family enzymes by cdk4 or cdk6, respectively, could induce either a pro- or anti-estrognic state in a breast tumor. The dashed blue lines indicate that the ER can interact with cyclin D1 to affect gene transcription, even in the absence of estrogen <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097448#pone.0097448-Neuman1" target="_blank">[40]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097448#pone.0097448-Zwijsen1" target="_blank">[41]</a>. The dashed black line indicates the interaction of the androgen receptor with cdk6, which can stimulate androgen receptor-directed gene transcription, independently of cyclin D1 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097448#pone.0097448-Lim2" target="_blank">[42]</a>. Steroid hormones bound to cognate steroid receptors regulate transcription of many genes that can affect tumor cell growth and function, including those encoding proteins that directly affect the cell cycle, such as c-myc and cyclin D1 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097448#pone.0097448-Dubik1" target="_blank">[38]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097448#pone.0097448-Altucci1" target="_blank">[39]</a> and perhaps SME genes themselves <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097448#pone.0097448-Kang1" target="_blank">[54]</a>.</p
The pattern of SME gene transcripts in breast cancer cells is largely independent of cyclin D1 levels.
<p>For panels (<b>A</b>) through (<b>C</b>), MDA-MB-468 breast epithelial cells were stably-transfected with a sequence encoding cyclin D1. (<b>A</b>) AKR1C1, AKR1C2, and AKR1C3 transcript levels in parental MDA-MB-468 cells (468) and in 3 stably-transfected cell lines (468-cyclin D1-1 through 468-cyclin D1-3) were detected and quantitated by qRT-PCR. (<b>B</b>) CYP19 and 17β-HSD2 transcript levels were similarly quantitated in the 4 cell lines. (<b>C</b>) The cyclin D1 protein levels in parental MDA-MB-468 cells and the 3 cyclin D1-transfectant cell lines analyzed in panels (<b>A</b>) and (<b>B</b>) were detected by immunoblot analysis, with β-actin levels as the loading control. For panels (<b>D</b>) and (<b>E</b>), MCF-7 breast epithelial cells were stably-transfected with a sequence encoding cyclin D1. (<b>D</b>) AKR1C1 and AKR1C3 transcript levels in parental MCF-7 cells and in 3 stably-transfected cell lines (MCF-7-cyclin D1-1 through MCF-7-cyclin D1–3) were detected and quantitated by qRT-PCR. (<b>E</b>) The cyclin D1 protein levels in parental MCF-7 and the 3 cyclin D1-transfectant cell lines analyzed in panel (<b>D</b>) were detected by immunoblot analysis, with β-actin levels as the loading control. For panels (<b>A</b>), (<b>B</b>), and (<b>D</b>), the data are expressed as the mean ± SEM, n = 3 times/group; *<i>p</i><0.05 and **<i>p</i><0.01. Note the differences in Y-axis scales on the graphs for panels (<b>A</b>), (<b>B</b>), and (<b>D</b>).</p