Seeking eye protection from biomass: Carbon dot-based optical blocking films with adjustable levels of blue light blocking.

The intensity of blue light in white light emitting diodes is typically higher than that of the green and red-light components in screen displays and lighting systems. To reduce the potential harm of in white light emitting diodes to the eyes, in this paper, we have used microcrystalline cellulose to synthesize biomass-based carbon dots (Bio-CD), which not only absorb short wavelength light to produce longer wavelength emissions, but also show concentration-dependent maximum excitation and maximum emission. The Bio-CDs were mixed with polyvinyl alcohol (PVA) to produce optical blocking films (OBF) that preferentially block blue light.

Biomass-Based Polymer Nanoparticles With Aggregation-Induced Fluorescence Emission for Cell Imaging and Detection of Fe Ions.

Polymeric nanoparticles, which show aggregation-induced luminescence emission, have been successfully prepared from larch bark, a natural renewable biomass resource, in a simple, rapid ultrasonic fragmentation method. The structure, element, particle size and molecular weight distribution of larch bark extracts (LBE) were studied by FTIR, XPS, TEM, XRD and linear mode mass spectrometry, respectively. LBE was found containing large numbers of aromatic rings, displaying an average particle size of about 4.

Preparation of Biomass-Based Carbon Dots with Aggregation Luminescence Enhancement from Hydrogenated Rosin for Biological Imaging and Detection of Fe.

Fluorescent carbon dots (CDs) have numerous important applications, but enhancing the fluorescence emission and overcoming fluorescence quenching are still big challenges. Here, fluorescence-enhanced carbon dots (named hr-CDs) were prepared from sustainable hydrogenated rosin, using a simple hydrothermal method in a water solvent. The hr-CDs were mainly composed of graphitized carbon cores with surface functional groups.

NPM1c impedes CTCF functions through cytoplasmic mislocalization in acute myeloid leukemia.

Normal cytogenetic acute myeloid leukemia (AML) frequently harbor a TCTG insertion in exon 12 of Nucleophosmin 1 (NPM1); the resulting frameshift creates a nuclear export signal (NES) and cytoplasmic localization of NPM1c. However, how NPM1c causes AML is not completely understood. NPM1 participates in multiple protein-protein interactions one of which involves the CCCTC-binding factor (CTCF).

SubID, a non-median dichotomization tool for heterogeneous populations, reveals the pan-cancer significance of INPP4B and its regulation by EVI1 in AML.

Our previous studies demonstrated that INPP4B, a member of the PI3K/Akt signaling pathway, is overexpressed in a subset of AML patients and is associated with lower response to chemotherapy and shorter survival. INPP4B expression analysis in AML revealed a right skewed frequency distribution with 25% of patients expressing significantly higher levels than the majority. The 75% low/25% high cut-off revealed the prognostic power of INPP4B expression status in AML, which would not have been apparent with a standard median cut-off approach.

Suspected leukemia oncoproteins CREB1 and LYL1 regulate Op18/STMN1 expression.

Stathmin (STMN1) is a microtubule destabilizing protein with a key role in cell cycle progression and cell migration that is up-regulated in several cancers and may contribute to the malignant phenotype. However, the factors that regulate its expression are not well understood. Loss as well as gain-of-function p53 mutations up-regulate STMN1 and in acute myelogenous leukemia where p53 is predominantly wild-type, STMN1 is also over-expressed.

FCHSD2 predicts response to chemotherapy in acute myeloid leukemia patients.

Acute myeloid leukemia (AML) is characterized by the growth and accumulation of cells blocked in their ability to differentiate, and blocks production of normal blood cells. The response to induction chemotherapy is heterogeneous, therefore biomarkers that predict for the outcome of such treatment are of potential value. FCHSD2 in a sensitized screen was identified as a potential chemo-protector (TW Mak, unpublished).

Wilms' tumor 1 suppressor gene mediates antiestrogen resistance via down-regulation of estrogen receptor-alpha expression in breast cancer cells.

The antiestrogen tamoxifen has been used in the treatment of hormone-responsive breast cancer for over a decade. The loss of estrogen receptor (ER) expression is the most common mechanism for de novo antiestrogen resistance. Wilms' tumor 1 suppressor gene (WT1) is a clinically useful marker that is associated with poor prognosis in breast cancer patients; its high level expression is frequently observed in cases of breast cancer that are estrogen and progesterone receptor negative.

Lyl1 interacts with CREB1 and alters expression of CREB1 target genes.

The basic helix-loop-helix (bHLH) transcription factor family contains key regulators of cellular proliferation and differentiation as well as the suspected oncoproteins Tal1 and Lyl1. Tal1 and Lyl1 are aberrantly over-expressed in leukemia as a result of chromosomal translocations, or other genetic or epigenetic events. Protein-protein and protein-DNA interactions described so far are mediated by their highly homologous bHLH domains, while little is known about the function of other protein domains.

The zinc finger domain of Wilms' tumor 1 suppressor gene (WT1) behaves as a dominant negative, leading to abrogation of WT1 oncogenic potential in breast cancer cells.

Introduction: There is growing evidence that the Wilms' tumor 1 suppressor gene (WT1) behaves as an oncogene in some forms of breast cancer. Previous studies have demonstrated that the N-terminal domain of WT1 can act as a dominant negative through self-association. In the studies presented here we have explored the potential for the zinc finger domain (ZF) of WT1 to also have dominant-negative effects, and thus further our understanding of this protein.

Transcriptional activation of c-myc proto-oncogene by WT1 protein.

The Wilms' tumor 1 gene (WT1) plays an essential role in urogenital development and malignancy. Through DNA binding, WT1 can either enhance or repress transcription depending on the context of the DNA-binding sites or the cell type in which it is expressed. WT1 is overexpressed in a variety of human cancers, including leukemia and breast cancer; in these diseases, the expression of WT1 is associated with a poor prognosis.