Silane Doping for Efficient Flexible Perovskite Solar Cells with Improved Defect Passivation and Device Stability

In this work, doping 3-amino-propyl triethoxysilane (APTES) into a perovskite precursor is proven to be an effective strategy, which can passivate crystal defects, control the crystallization rate, and improve the morphology. APTES can form oligomers through hydrolysis and a condensation reaction, thus blocking the invasion of external water molecules. In addition, the lone pair electrons on the N atom in the amino group of APTES form a coordination bond with perovskite by sharing the empty 6p orbital on Pb2+, which can effectively passivate the defects of the film and realize a highly uniform and dense perovskite film with preferential crystal growth orientation. The film exhibits high (110) crystal plane orientation and long carrier lifetime and mobility, which improves the performance of flexible perovskite solar cells. Using this approach, the champion device presents an optimal power conversion efficiency of 19.84% with much promoted air stability. Moreover, the efficiency of flexible devices does not decrease after maximum power point irradiation for 360 s

Additional file 1 of pH- and acoustic-responsive platforms based on perfluoropentane-loaded protein nanoparticles for ovarian tumor-targeted ultrasound imaging and therapy

Additional file 1: Figure S1. The FT-IR spectrum of FA-FRT. Figure S2. The statistical data of FITC fluorescence signal inside HUM-CELL-0088 cells treated with free FITC and FITC labeled FRT-PFP, FA-FRT-PFP + FA and FA-FRT-PFP. Figure S3. Cell viabilities of HUM-CELL-0088 cells treated with 40 μg/ml of PBS (control), FRT-PFP, FA-FRT-PFP + FA and FA-FRT-PFP combined with or without LIFU irradiation (2.0 W/cm2, 4 min) and further 21 h incubation. Figure S4. The TNF protein expression level of cells treated with 40 μg/mL of PBS (control), FRT-PFP, FA-FRT-PFP + FA and FA-FRT-PFP combined with or without LIFU irradiation (2.0 W/cm2, 4 min) and further 21 h incubation

Summary statistics: household characteristics for the whole cohort and subgroups with different illness conditions.

<p>Summary statistics: household characteristics for the whole cohort and subgroups with different illness conditions.</p

Sulindac modulates secreted protein expression from LIM1215 colon carcinoma cells prior to apoptosis

Colorectal cancer (CRC) is a major cause of mortality in Western populations. Growing evidence from human and rodent studies indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) cause regression of existing colon tumors and act as effective chemopreventive agents in sporadic colon tumor formation. Although much is known about the action of the NSAID sulindac, especially its role in inducing apoptosis, mechanisms underlying these effects is poorly understood. In previous secretome-based proteomic studies using 2D-DIGE/MS and cytokine arrays we identified over 150 proteins released from the CRC cell line LIM1215 whose expression levels were dysregulated by treatment with 1 mM sulindac over 16 h; many of these proteins are implicated in molecular and cellular functions such as cell proliferation, differentiation, adhesion, angiogenesis and apoptosis (Ji et al., Proteomics Clin. Appl. 2009, 3, 433-451). We have extended these studies and describe here an improved protein/peptide separation strategy that facilitated the identification of 987 proteins and peptides released from LIM1215 cells following 1 mM sulindac treatment for 8 h preceding the onset of apoptosis. This peptidome separation strategy involved fractional centrifugal ultrafiltration of concentrated cell culture media (CM) using nominal molecular weight membrane filters (NMWL 30 K, 3 K and 1 K). Proteins isolated in the > 30 K and 3-30 K fractions were electrophoretically separated by SDS-PAGE and endogenous peptides in the 1-3 K membrane filter were fractioned by RP-HPLC; isolated proteins and peptides were identified by nanoLC-MS-MS. Collectively, our data show that LIM1215 cells treated with 1 mM sulindac for 8 h secrete decreased levels of proteins associated with extracellular matrix remodeling (e.g., collagens, perlecan, syndecans, filamins, dyneins, metalloproteinases and endopeptidases), cell adhesion (e.g., cadherins, integrins, laminins) and mucosal maintenance (e.g., glycoprotein 340 and mucins 5 AC, 6, and 13). A salient finding of this study was the increased proteolysis of cell surface proteins following treatment with sulindac for 8 h (40% higher than from untreated LIM1215 cells); several of these endogenous peptides contained C-terminal amino acids from transmembrane domains indicative of regulated intramembrane proteolysis (RIP). Taken together these results indicate that during the early-stage onset of sulindac-induced apoptosis (evidenced by increased annexin V binding, dephosphorylation of focal adhesion kinase (FAK), and cleavage of caspase-3), 1 mM sulindac treatment of LIM1215 cells results in decreased expression of secreted proteins implicated in ECM remodeling, mucosal maintenance and cell-cell-adhesion. This article is part of a Special Issue entitled: An Updated Secretome. © 2013 Elsevier B.V

Multivariate linear regression analysis of per capita medical expense.

<p>In each cell, regression coefficient (p-value).Other occupation includes: government, student, self-employed, public or private company and others.</p

Multivariate analysis of the percentage of per capita medical expense (as of per capita total expense).

<p>In each cell, odds ratio (p-value). Other occupation includes: government, student, self-employed, public or private company and others.</p

Multivariate logistic regression analysis of illness conditions.

<p>In each cell, odds ratio (p-value). Inpatient: presence of inpatient treatment for a household; Outpatient: per person outpatient treatments>2; Self-treatment: per person self-treatment>5. Other occupation includes: government, student, self-employed, public or private company and others.</p

Summary statistics: household head characteristics for the whole cohort and subgroups with different illness conditions.

*<p>Other occupation includes: government, student, self-employed, public or private company and others.</p

Table1_Case report: Composite mantle cell lymphoma and classical Hodgkin lymphoma.docx

Composite mantle cell lymphoma and classical Hodgkin lymphoma is very rare and the actual origin of it is still unclear. Here we reported a new case of composite mantle cell lymphoma and classical Hodgkin lymphoma and analyzed its molecular changes. Eight mutations were identified in its Hodgkin component through next-generation sequencing. In addition, we reviewed the published cases of composite mantle cell lymphoma and classical Hodgkin lymphoma and summarized the molecular changes of reported cases as well as the current case to explore the possible pathway of histogenesis.</p

Exosomes Derived from Human Primary and Metastatic Colorectal Cancer Cells Contribute to Functional Heterogeneity of Activated Fibroblasts by Reprogramming Their Proteome

Cancer-associated fibroblasts (CAFs) are a heterogeneous population of activated fibroblasts that constitute a dominant cellular component of the tumor microenvironment (TME) performing distinct functions. Here, the role of tumor-derived exosomes (Exos) in activating quiescent fibroblasts into distinct functional subtypes is investigated. Proteomic profiling and functional dissection reveal that early- (SW480) and late-stage (SW620) colorectal cancer (CRC) cell-derived Exos both activated normal quiescent fibroblasts (α-SMA − , CAV + , FAP + , VIM + ) into CAF-like fibroblasts (α-SMA + , CAV − , FAP + , VIM + ). Fibroblasts activated by early-stage cancer-exosomes (SW480-Exos) are highly pro-proliferative and pro-angiogenic and display elevated expression of pro-angiogenic (IL8, RAB10, NDRG1) and pro-proliferative (SA1008, FFPS) proteins. In contrast, fibroblasts activated by late-stage cancer-exosomes (SW620-Exos) display a striking ability to invade through extracellular matrix through upregulation of pro-invasive regulators of membrane protrusion (PDLIM1, MYO1B) and matrix-remodeling proteins (MMP11, EMMPRIN, ADAM10). Conserved features of Exos-mediated fibroblast activation include enhanced ECM secretion (COL1A1, Tenascin-C/X), oncogenic transformation, and metabolic reprogramming (downregulation of CAV-1, upregulation of glycogen metabolism (GAA), amino acid biosynthesis (SHMT2, IDH2) and membrane transporters of glucose (GLUT1), lactate (MCT4), and amino acids (SLC1A5/3A5)). This study highlights the role of primary and metastatic CRC tumor-derived Exos in generating phenotypically and functionally distinct subsets of CAFs that may facilitate tumor progression