Miracle-dz/UniFAR-FTUs huggingface dataset:
Influence of Clay Surface Modification on Morphology and Rheology of Polyethylene Glycol/Montmorillonite Nanocomposites

The effects of surface modification of Na-montmorillonite (Na-MMT) on morphology and the rheological properties of polyethylene glycol/ organoclay nanocomposites are investigated. Dodecyltrimethylammonium bromide (DTABr) is used to modify the clay surface. Adsorption of DTABr on Na-MMT is monitored by zeta potential measurements. From zeta potential measurements, three DTABr concentrations, 1 × 10—3, 7.5 × 10— 3, and 5 × 10—2 mol/L, are chosen to fabricate the polyethylene glycol/organoclay composites. The morphology of three sets of organoclays (OMMT1, OMMT2, and OMMT3) is studied by X-ray diffraction (XRD) technique. The increase of basal spacing is found to be 0.2 nm as the DTABr concentration is increased to 7.5 × 10— 3 mol/L. The rheological properties of polyethylene glycol (PEG)/ organoclay nanocomposites are studied for three organoclays at different PEG concentrations. All nanocomposites show Bingham plastic flow behavior. The OMMT3 shows maximum viscoelastic properties in the polymer matrix. The morphology and electrokinetic properties of the PEG/organoclay nanocomposites are also investigated.
From Structure to Function with Binding Free Energy Calculations for Codon Reading, Riboswitches and Lectins

The linear interaction energy (LIE) method to compute binding free energies is applied to lectin-monosaccharide complexes. Here, we calculate the binding free energies of monosaccharides to the Ralstonia solanacearum lectin (RSL) and the Pseudomonas aeruginosa lectin-II (PA-IIL). The standard LIE model performs very well for RSL, whereas the PA-IIL system, where ligand binding involves two calcium ions, presents a major challenge. To overcome this, we explore a new variant of the LIE model, where ligandmetal ion interactions are scaled separately. This model also predicts the saccharide binding preference of PA-IIL on mutation of the receptor, which may be useful for protein engineering of lectins.
Human Intellectual Disability Genes Form Conserved Functional Modules in Drosophila

Intellectual Disability (ID) disorders, defined by an IQ below 70, are genetically and phenotypically highly heterogeneous. Identification of common molecular pathways underlying these disorders is crucial for understanding the molecular basis of cognition and for the development of therapeutic intervention strategies. To systematically establish their functional connectivity, we used transgenic RNAi to target 270 ID gene orthologs in the Drosophila eye. Assessment of neuronal function in behavioral and electrophysiological assays and multiparametric morphological analysis identified phenotypes associated with knockdown of 180 ID gene orthologs. Most of these genotype-phenotype associations were novel. For example, we uncovered 16 genes that are required for basal neurotransmission and have not previously been implicated in this process in any system or organism. ID gene orthologs with morphological eye phenotypes, in contrast to genes without phenotypes, are relatively highly expressed in the human nervous system and are enriched for neuronal functions, suggesting that eye phenotyping can distinguish different classes of ID genes. Indeed, grouping genes by Drosophila phenotype uncovered 26 connected functional modules. Novel links between ID genes successfully predicted that MYCN, PIGV and UPF3B regulate synapse development. Drosophila phenotype groups show, in addition to ID, significant phenotypic similarity also in humans, indicating that functional modules are conserved. The combined data indicate that ID disorders, despite their extreme genetic diversity, are caused by disruption of a limited number of highly connected functional modules.
On the performance analysis of digital communications over generalized-K fading channels

The performance of digital communication systems over generalized-K (K/sub G/) fading channels is analyzed and evaluated. Novel closed form expressions for the SNR statistics, the average Shannon's channel capacity and the bit error rate (BER) are derived. These expressions are used to study important performance criteria such as the outage performance, the average capacity and the BER for a great variety of modulation formats in K/sub G/ fading channels. The proposed mathematical analysis is accompanied with various performance evaluation results, which demonstrate the usefulness of the proposed approach.
Practical Problems With Clinical Guidelines for Breast Cancer Prevention Based on Remaining Lifetime Risk

Background: Clinical guidelines for breast cancer chemoprevention and MRI screening involve estimates of remaining lifetime risk (RLR); in the United States, women with an RLR of 20% or higher meet “high-risk” criteria for MRI screening. Methods: We prospectively followed 1764 women without breast cancer to compare the RLRs and 10-year risks assigned by the risk models International Breast Cancer Intervention Study (IBIS) and Breast and Ovarian Analysis of Disease Incidence and Carrier Estimation Algorithm (BOADICEA) and to compare both sets of model-assigned 10-year risks to subsequent incidence of breast cancer in the cohort. We used chi-square statistics to assess calibration and the area under the receiver operating characteristic curve (AUC) to assess discrimination. All statistical tests are two-sided. Results: The models classified different proportions of women as high-risk (IBIS = 59.3% vs BOADICEA = 20.1%) using the RLR threshold of 20%. The difference was smaller (IBIS = 52.9% vs BOADICEA = 43.2%) using a 10-year risk threshold of 3.34%. IBIS risks (mean = 4.9%) were better calibrated to observed breast cancer incidence (5.2%, 95% confidence interval (CI) = 4.2% to 6.4%) than were those of BOADICEA (mean = 3.7%) overall and within quartiles of model risk (P = .20 by IBIS and P = .07 by BOADICEA). Both models gave similar discrimination, with AUCs of 0.67 (95% CI = 0.61 to 0.73) using IBIS and 0.68 (95% CI = 0.62 to 0.74) using BOADICEA. Model sensitivities at thresholds for a 20% false-positive rate were also similar, with 41.8% using IBIS and 38.0% using BOADICEA. Conclusion: RLR-based guidelines for high-risk women are limited by discordance between commonly used risk models. Guidelines based on short-term risks would be more useful, as models are generally developed and validated under a short fixed time horizon (≤10 years).
Synthesis of nano CaCO3/acrylic co‐polymer latex composites for interior decorative paints

CaCO3 nanoparticles were synthesised in patented solution spray reactor system using non-ionic Tween-80 surfactant as template. Design of solution spray reactor permits the intimate thin film contact between the highly atomized precursor and precipitant solutions to control the CaCO3 size in 25-90 nm range. CaCO3 nanoparticles were surface modified with γ-methacryloxypropyltrimethoxysilane (GMPTS) in order to improve the compatibility with polymer matrix. CaCO3/acrylic co-polymer latex nanocomposites were prepared by in situ emulsion polymerization with 0.5-2.5 wt % loadings of nanoCaCO3. Functional group, surface modification, crystal phase, size and morphology of CaCO3 nanoparticles were determined by their FTIR, XRD and FESEM analysis. DSC and TGA analysis was performed to establish the rise in thermal stability of latex nanocomposites due to inclusion of nanoCaCO3, while its ultrafine dispersion in polymer matrix was confirmed by FESEM analysis of latex nanocomposite films. Interior waterborne decorative paints were formulated using CaCO3/acrylic co-polymer latex nanocomposites as binder. Overall three fold rise in performance of latex nanocomposite paint over that of clear latex paint in terms of wet scrub, mar and stain resistance, cross cut adhesion and pencil hardness was observed which implies commercial viability of use of surface modified nanoCaCO3. POLYM. COMPOS. , 00:000–000, 2016. © 2016 Society of Plastics Engineers
The MicroRNA-21 signaling pathway is involved in prorenin receptor (PRR) –induced VEGF expression in ARPE-19 cells under a hyperglycemic condition

Purpose MicroRNAs (miRNAs/miRs) are involved in a large number of biological functions and diseases, such as cancer, cardiovascular diseases, and diabetes. MiR-21 has been reported to target Sprouty homolog 1 (SPRY1), SMAD7, and PTEN. In this study, we examined the underlying role of miR-21 in the regulation of prorenin receptor (PRR)-mediated induction of vascular endothelial growth factor (VEGF) expression via targeting SMAD7, SPRY1, and PTEN in a hyperglycemic condition. Methods PRR-mediated induction of VEGF under a hyperglycemic condition (high glucose, 33mM) was studied by treating ARPE-19 cells with perindopril (10 µmol/l), which inhibits angiotensin II-mediated signaling. ARPE-19 cells exposed to normal glucose (NG, 5.5 mM) were considered as the control. To examine the role of miR-21 in the regulation of SPRY1, SMAD7, PTEN, and VEGF, ARPE-19 cells cultured in NG or high glucose were transfected with scramble negative control (Scr), a miR-21 mimic, or a miR-21 antagomir. To investigate the role of PRR and the small GTP-binding protein RAC1 in the regulation of miR-21, the expression of PRR and RAC1 was silenced by transfecting ARPE-19 cells with their corresponding siRNAs. Results Compared with the NG control, high glucose significantly induced the expression of PRR, VEGF, VEGFR2, and miR-21 but significantly suppressed the expression of SPRY1, SMAD7, and PTEN at the transcript and protein levels. In contrast, silencing the expression of PRR significantly abolished the high glucose–induced expression of VEGF, VEGFR2, and miR-21. Knockdown of RAC1 significantly attenuated the high glucose–induced expression of LOX, CTGF, and miR-21, suggesting that PRR and RAC1 are involved in the CTGF/LOX-mediated regulation of miR-21. Furthermore, high glucose dramatically increased the levels of pERK (p44), hypoxia-inducible factor (HIF-1α), and VEGF. However, this effect was antagonized by the miR-21 antagomir, indicative of the involvement of high glucose–induced miR-21 in the regulation of VEGF through ERK signaling. Conclusions Our findings, for the first time, showed that the pleiotropic action of miR-21 induced the expression of pERK, HIF-1α, and VEGF in the high glucose condition by simultaneously targeting SPRY1, SMAD7, and PTEN in ARPE-19 cells. Therefore, miR-21 may serve as a potential therapeutic target for diabetes-induced retinal pathology.
Use of Nanotechnologies for Drug Delivery

The emerging field of nanotechnology has an enormous potential contribution to make to the field of pharmaceutical materials science. The advantages of drug nanoparticles can be as simple as dissolution rate enhancement through increased surface area or as complex as targeted delivery through novel pathways. However, the application of many nanoscale technologies has been slow because of difficulties controlling the drug form with decreasing particle size and maintaining chemical and physical stability upon storage. Advancing beyond these limitations requires a unique understanding of both the material properties of the active ingredients as well as the physical chemistry of the nano-sized particle. This article will examine the current challenges facing the pharmaceutical industry in applying nanotechnology, with a focus on the deficiencies in understanding that need to be addressed to move forward.
Ancestral xerophobia: a hypothesis on the whole plant ecophysiology of early angiosperms

Today, angiosperms are fundamental players in the diversity and biogeochemical functioning of the planet. Yet despite the omnipresence of angiosperms in today's ecosystems, the basic evolutionary understanding of how the earliest angiosperms functioned remains unknown. Here we synthesize ecophysiological, paleobotanical, paleoecological, and phylogenetic lines of evidence about early angiosperms and their environments. In doing so, we arrive at a hypothesis that early angiosperms evolved in evermoist tropical terrestrial habitats, where three of their emblematic innovations – including net‐veined leaves, xylem vessels, and flowers – found ecophysiological advantages. However, the adaptation of early angiosperm ecophysiology to wet habitats did not initially promote massive diversification and ecological dominance. Instead, wet habitats were permissive for the ecological roothold of the clade, a critical phase of early diversification that entailed experimentation with a range of functional innovations in the leaves, wood, and flowers. Later, our results suggest that some of these innovations were co‐opted gradually for new roles in the evolution of greater productivity and drought tolerance, which are characteristics seen across the vast majority of derived and ecologically dominant angiosperms today.
The failure of oral tolerance induction is functionally coupled to the absence of T cells in Peyer's patches under germfree conditions.

Although intestinal bacterial flora has been thought to play a role in the induction of oral tolerance, the mechanism has yet to be elucidated. We therefore examined the bacterial flora-dependent acquisition of susceptibility to oral tolerance induction using a gnotobiotic murine model. Germ-free (GF) mice exhibited a significant shortage of T cells in the PPs in comparison to SPF mice. A recovery in the number of such T cells was accomplished in the gnotobiotic mice associated with Bifidobacterium infantis or Escherichia coli but not in the gnotobiotic mice with Clostridium perfringens or Staphylococcus aureus. To examine the susceptibility to oral tolerance induction, these mice were orally given ovalbumin (OVA) as a tolerogen and then injected i.p. with the Ag. The Ag-specific IgG1 in the serum remained at a low level in both SPF and those gnotobiotic mice groups containing a sufficient number of T cells in the PPs. However, no such unresponsiveness in the Ab response was observed in GF or the other gnotobiotic mice groups containing only a few T cells in the tissues. Adoptive cell transfer analysis clearly showed that a sufficient number of T cells in the PPs is required for the induction of oral tolerance. Furthermore, the reduced expression of SLC (secondary lymphoid-tissue chemokine), which is responsible for T-cell migration to lymphoid organs, was observed in the PPs of GF mice, resulting in a shortage of T cells in the tissues. However, the reduced expression of SLC was restored even in the GF mice after conventionalization, thus suggesting that the failure of oral tolerance induction is functionally coupled to the innate absence of T cells under the GF condition.
Up-regulation of microRNA-367 promotes liver steatosis through repressing TBL1 in obese mice.

OBJECTIVE Increasing evidence has demonstrated that microRNAs (miRNAs) play a critical role in the progression of metabolic disorders, including obesity-induced non-alcoholic fatty liver disease (NAFLD). In the present study, the expression and function of miR-367 were investigated. MATERIALS AND METHODS C57BL/6 male mice aged 8 weeks were fed with a normal diet (ND) or high-fat-diet (HFD). The expression levels of miR-367 were analyzed in livers from two groups of mice by quantitative real-time PCR. Adenovirus containing miR-367 or negative control (NC) were constructed and administrated into C57BL/6 mice by tail vain injection. Potential targets of miR-367 were screened by miRWalk software and luciferase reporter assays. Mutagenesis analysis and Western blots were used to further determine the target of miR-367 in obese mice. RESULTS We found that the expression of hepatic miR-367 was up-regulated in obese mice. In vitro and in vivo studies further demonstrated that overexpression of miR-367 mimics promoted triglyceride accumulation in cells and lean mice. At the molecular level, transducin beta-like 1 (TBL1), a coactivator of nuclear receptor peroxisome proliferator-activated receptor (PPAR) α, was identified as a direct target of miR-367. As a result, miR-367 overexpression resulted in an inhibition of fatty acid oxidation, leading to hepatosteatosis. CONCLUSIONS Our data suggest miR-367/TBL1 regulatory pathway might have an important role for in the development of NAFLD.
From therapeutic antibodies to chimeric antigen receptors (CARs): making better CARs based on antigen-binding domain

ABSTRACT Introduction: A variety of approaches are being pursued to improve the safety and antitumor potency of chimeric antigen receptor (CAR) T-cell therapy. However, most engineering efforts have thus far been focused on its intracellular signaling domain, while its extracellular antigen-binding domain has received less attention. Areas covered: Herein, the authors summarize the current knowledge of CAR T-cell therapy. Accordingly, they focus on its antigen-binding domain, discuss key considerations for selecting an optimal single-chain variable fragment (scFv) when designing a CAR, and suggest potential directions aimed at developing the next-generation CARs. Expert opinion: The extracellular region of CARs can play a decisive role in their safety and efficacy. Instead of directly translating an available therapeutic mAb to a scFv-based CAR construct, the authors suggest that various CAR-displayed scFvs with different affinity, specificity and binding epitopes against an individual target molecule should be generated and evaluated side-by-side. Incorporating new antibody formats that possess characteristics superior to those of scFvs may be one way to engineer safer and more effective CARs. The authors expect that further CAR engineering will enable us to target more antigens involved in hematological and solid malignancies with minimal side effects to serve unmet clinical needs.
Quantifying the Effects of Compressive Loads on the Heat Generation of Prismatic Lithium-ion Pouch Cells

The proper design for a battery thermal management system (BTMS) in an electric or hybrid electric vehicle requires that all of the factors which affect heat generation within the battery cell be fully understood. Much research has been published that establishes the relationship between the rate of heat generation of a cell to its temperature, state-of-charge (SOC), and rate of charge or discharge. However, there is one factor that has mostly escaped the same level of intense scrutiny in published literature as the others: cell compression.
Hsp70–Hsp110 chaperones deliver ubiquitin-dependent and -independent substrates to the 26S proteasome for proteolysis in yeast

ABSTRACT During protein quality control, proteotoxic misfolded proteins are recognized by molecular chaperones, ubiquitylated by dedicated quality control ligases and delivered to the 26S proteasome for degradation. Proteins belonging to the Hsp70 chaperone and Hsp110 (the Hsp70 nucleotide exchange factor) families function in the degradation of misfolded proteins by the ubiquitin-proteasome system via poorly understood mechanisms. Here, we report that the Saccharomyces cerevisiae Hsp110 proteins (Sse1 and Sse2) function in the degradation of Hsp70-associated ubiquitin conjugates at the post-ubiquitylation step and are also required for ubiquitin-independent proteasomal degradation. Hsp110 associates with the 19S regulatory particle of the 26S proteasome and interacts with Hsp70 to facilitate the delivery of Hsp70 substrates for proteasomal degradation. By using a highly defined ubiquitin-independent proteasome substrate, we show that the mere introduction of a single Hsp70-binding site renders its degradation dependent on Hsp110. The findings define a dedicated and chaperone-dependent pathway for the efficient shuttling of cellular proteins to the proteasome with profound implications for understanding protein quality control and cellular stress management. Summary: Hsp110 associates with the proteasome and ensures the efficient delivery of Hsp70 chaperone-associated proteins for proteolysis in the yeast S. cerevisiae.
Circulating ACE2 activity correlates with cardiovascular disease development

It was shown recently that angiotensin-converting enzyme activity is limited by endogenous inhibition in vivo, highlighting the importance of angiotensin II (ACE2) elimination. The potential contribution of the ACE2 to cardiovascular disease progression was addressed. Serum ACE2 activities were measured in different clinical states (healthy, n=45; hypertensive, n=239; heart failure (HF) with reduced ejection fraction (HFrEF) n=141 and HF with preserved ejection fraction (HFpEF) n=47). ACE2 activity was significantly higher in hypertensive patients (24.8±0.8 U/ml) than that in healthy volunteers (16.2±0.8 U/ml, p=0.01). ACE2 activity further increased in HFrEF patients (43.9±2.1 U/ml, p=0.001) but not in HFpEF patients (24.6±1.9 U/ml) when compared with hypertensive patients. Serum ACE2 activity negatively correlated with left ventricular systolic function in HFrEF, but not in hypertensive, HFpEF or healthy populations. Serum ACE2 activity had a fair diagnostic value to differentiate HFpEF from HFrEF patients in this study. Serum ACE2 activity correlates with cardiovascular disease development: it increases when hypertension develops and further increases when the cardiovascular disease further progresses to systolic dysfunction, suggesting that ACE2 metabolism plays a role in these processes. In contrast, serum ACE2 activity does not change when hypertension progresses to HFpEF, suggesting a different pathomechanism for HFpEF, and proposing a biomarker-based identification of these HF forms.
Mitochondrial BK Channel Openers CGS7181 and CGS7184 Exhibit Cytotoxic Properties

Potassium channel openers (KCOs) have been shown to play a role in cytoprotection through the activation of mitochondrial potassium channels. Recently, in several reports, a number of data has been described as off-target actions for KCOs. In the present study, we investigated the effects of BKCa channel openers CGS7181, CGS7184, NS1619, and NS004 in neuronal cells. For the purpose of this research, we used a rat brain, the mouse hippocampal HT22 cells, and the human astrocytoma U-87 MG cell line. We showed that CGS7184 activated the mitochondrial BKCa (mitoBKCa) channel in single-channel recordings performed on astrocytoma mitoplasts. Moreover, when applied to the rat brain homogenate or isolated rat brain mitochondria, CGS7184 increased the oxygen consumption rate, and can thus be considered a potentially cytoprotective agent. However, experiments on intact neuronal HT22 cells revealed that both CGS7181 and CGS7184 induced HT22 cell death in a concentration- and time-dependent manner. By contrast, we did not observe cell death when NS1619 or NS004 was applied. CGS7184 toxicity was not abolished by BKCa channel inhibitors, suggesting that the observed effects were independent of a BKCa-type channel activity. CGS7184 treatment resulted in an increase of cytoplasmic Ca2+ concentration that likely involved efflux from internal calcium stores and the activation of calpains (calcium-dependent proteases). The cytotoxic effect of the channel opener was partially reversed by a calpain inhibitor. Our data show that KCOs under study not only activate mitoBKCa channels from brain tissue, but also induce cell death when used in cellular models.
Back-contacted hybrid organic–inorganic perovskite solar cells

A novel architecture for quasi-interdigitated electrodes (QIDEs) allows for the fabrication of back-contacted perovskite solar cells. The devices showed a stable power output of 3.2%. The design of the QIDEs avoids the defects that cause short-circuiting in conventional IDEs, while enhancing the collection area of the electrodes. Photoluminescence and photocurrent mapping is used to probe the charge generation and transport properties of the perovskite solar cells.