569 research outputs found
Impact of the IEC (Information, Education and Communication) activities under the Christian Service-Learning Program of the Communication Department of the University of St. La Salle on the Muslim community in Bacolod City, Philippines
Phonons of Metallic Vicinal Surfaces
We present an analysis of the vibrational dynamics of metal vicinal surfaces
using the embedded atom method to describe the interaction potential and both a
real space Green's function method and a slab method to calculate the phonons.
We report two main general characteristics : a global shift of the surface
vibrational density of states resulting from a softening of the force field.
The latter is a direct result of the reduction of coordination for the
different type of surface atoms; and an appearance of high frequency modes
above the bulk band, resulting from a stiffening of the force field near the
step atom. The latter is due to a rearrangement of the atomic positions during
the relaxation of the surface atoms yielding a large shortening of the nearest
neighbor distances near the step atoms.Comment: 6 figures, to appear in Sur. Sci. proceedings of VAS1
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Monitoring Motor Fluctuations in Patients With Parkinson’s Disease Using Wearable Sensors
This paper presents the results of a pilot study to
assess the feasibility of using accelerometer data to estimate the
severity of symptoms and motor complications in patients with
Parkinson’s disease. A support vector machine (SVM) classifier
was implemented to estimate the severity of tremor, bradykinesia
and dyskinesia from accelerometer data features. SVM-based
estimates were compared with clinical scores derived via visual inspection
of video recordings taken while patients performed a series
of standardized motor tasks. The analysis of the video recordings
was performed by clinicians trained in the use of scales for the
assessment of the severity of Parkinsonian symptoms and motor
complications. Results derived from the accelerometer time series
were analyzed to assess the effect on the estimation of clinical scores
of the duration of the window utilized to derive segments (to eventually
compute data features) from the accelerometer data, the use
of different SVM kernels and misclassification cost values, and the
use of data features derived from different motor tasks. Results
were also analyzed to assess which combinations of data features
carried enough information to reliably assess the severity of symptoms
andmotor complications.Combinations of data features were
compared taking into consideration the computational cost associated
with estimating each data feature on the nodes of a body
sensor network and the effect of using such data features on the
reliability of SVM-based estimates of the severity of Parkinsonian
symptoms and motor complications.Engineering and Applied Science
Coexisting conical bipolar and equatorial outflows from a high-mass protostar
The BN/KL region in the Orion molecular cloud is an archetype in the study of
the formation of stars much more massive than the Sun. This region contains
luminous young stars and protostars, but it is difficult to study because of
overlying dust and gas. Our basic expectations are shaped to some extent by the
present theoretical picture of star formation, the cornerstone of which is that
protostars acrete gas from rotating equatorial disks, and shed angular momentum
by ejecting gas in bipolar outflows. The main source of the outflow in the
BN/KL region may be an object known as radio source I, which is commonly
believed to be surrounded by a rotating disk of molecular material. Here we
report high-resolution observations of silicon monoxide (SiO) and water maser
emission from the gas surrounding source I; we show that within 60 AU (about
the size of the Solar System), the region is dominated by a conical bipolar
outflow, rather than the expected disk. A slower outflow, close to the
equatorial plane of the protostellar system, extends to radii of 1,000 AU.Comment: 10 pages, 2 figures. Accepted by Nature. To appear December 199
TGF-beta 1 induces human alveolar epithelial to mesenchymal cell transition (EMT)
Background: Fibroblastic foci are characteristic features in lung parenchyma of patients with idiopathic pulmonary fibrosis (IPF). They comprise aggregates of mesenchymal cells which underlie sites of unresolved epithelial injury and are associated with progression of fibrosis. However, the cellular origins of these mesenchymal phenotypes remain unclear. We examined whether the potent fibrogenic cytokine TGF-β1 could induce epithelial mesenchymal transition (EMT) in the human alveolar epithelial cell line, A549, and investigated the signaling pathway of TGF-β1-mediated EMT.
Methods: A549 cells were examined for evidence of EMT after treatment with TGF-β1. EMT was assessed by: morphology under phase-contrast microscopy; Western analysis of cell lysates for expression of mesenchymal phenotypic markers including fibronectin EDA (Fn-EDA), and expression of epithelial phenotypic markers including E-cadherin (E-cad). Markers of fibrogenesis, including collagens and connective tissue growth factor (CTGF) were also evaluated by measuring mRNA level using RT-PCR, and protein by immunofluorescence or Western blotting. Signaling pathways for EMT were characterized by Western analysis of cell lysates using monoclonal antibodies to detect phosphorylated Erk1/2 and Smad2 after TGF-β1 treatment in the presence or absence of MEK inhibitors. The role of Smad2 in TGF-β1-mediated EMT was investigated using siRNA.
Results: The data showed that TGF-β1, but not TNF-α or IL-1β, induced A549 cells with an alveolar epithelial type II cell phenotype to undergo EMT in a time-and concentration-dependent manner. The process of EMT was accompanied by morphological alteration and expression of the fibroblast phenotypic markers Fn-EDA and vimentin, concomitant with a downregulation of the epithelial phenotype marker E-cad. Furthermore, cells that had undergone EMT showed enhanced expression of markers of fibrogenesis including collagens type I and III and CTGF. MMP-2 expression was also evidenced. TGF-β1-induced EMT occurred through phosphorylation of Smad2 and was inhibited by Smad2 gene silencing; MEK inhibitors failed to attenuate either EMT-associated Smad2 phosphorylation or the observed phenotypic changes.
Conclusion: Our study shows that TGF-β1 induces A549 alveolar epithelial cells to undergo EMT via Smad2 activation. Our data support the concept of EMT in lung epithelial cells, and suggest the need for further studies to investigate the phenomenon
Dasatinib inhibits CXCR4 signaling in chronic lymphocytic leukaemia cells and impairs migration towards CXCL12
Chemokines and their ligands play a critical role in enabling chronic lymphocytic leukaemia (CLL) cells access to protective microenvironmental niches within tissues, ultimately resulting in chemoresistance and relapse: disruption of these signaling pathways has become a novel therapeutic approach in CLL. The tyrosine kinase inhibitor dasatinib inhibits migration of several cell lines from solid-organ tumours, but effects on CLL cells have not been reported. We studied the effect of clinically achievable concentrations of dasatinib on signaling induced by the chemokine CXCL12 through its' receptor CXCR4, which is highly expressed on CLL cells. Dasatinib pre-treatment inhibited Akt and ERK phosphorylation in CLL cells upon stimulation with CXCL12. Dasatinib also significantly diminished the rapid increase in actin polymerisation observed in CLL cells following CXCL12 stimulation. Moreover, the drug significantly inhibited chemotaxis in a transwell assay, and reduced the percentage of cells able to migrate beneath a CXCL12-expressing murine stromal cell line. Dasatinib also abrogated the anti-apoptotic effect of prolonged CXCL12 stimulation on cultured CLL cells. These data suggest that dasatinib, akin to other small molecule kinase inhibitors targeting the B-cell receptor signaling pathway, may redistribute CLL cells from protective tissue niches to the peripheral blood, and support the investigation of dasatinib in combination strategies
Identifying metabolites by integrating metabolome databases with mass spectrometry cheminformatics.
Novel metabolites distinct from canonical pathways can be identified through the integration of three cheminformatics tools: BinVestigate, which queries the BinBase gas chromatography-mass spectrometry (GC-MS) metabolome database to match unknowns with biological metadata across over 110,000 samples; MS-DIAL 2.0, a software tool for chromatographic deconvolution of high-resolution GC-MS or liquid chromatography-mass spectrometry (LC-MS); and MS-FINDER 2.0, a structure-elucidation program that uses a combination of 14 metabolome databases in addition to an enzyme promiscuity library. We showcase our workflow by annotating N-methyl-uridine monophosphate (UMP), lysomonogalactosyl-monopalmitin, N-methylalanine, and two propofol derivatives
Inhibiting ERK Activation with CI-1040 Leads to Compensatory Upregulation of Alternate MAPKs and Plasminogen Activator Inhibitor-1 following Subtotal Nephrectomy with No Impact on Kidney Fibrosis
Extracellular-signal regulated kinase (ERK) activation by MEK plays a key role in many of the cellular processes that underlie progressive kidney fibrosis including cell proliferation, apoptosis and transforming growth factor β1-mediated epithelial to mesenchymal transition. We therefore assessed the therapeutic impact of ERK1/2 inhibition using a MEK inhibitor in the rat 5/6 subtotal nephrectomy (SNx) model of kidney fibrosis. There was a twentyfold upregulation in phospho-ERK1/2 expression in the kidney after SNx in Male Wistar rats. Rats undergoing SNx became hypertensive, proteinuric and developed progressive kidney failure with reduced creatinine clearance. Treatment with the MEK inhibitor, CI-1040 abolished phospho- ERK1/2 expression in kidney tissue and prevented phospho-ERK1/2 expression in peripheral lymphocytes during the entire course of therapy. CI-1040 had no impact on creatinine clearance, proteinuria, glomerular and tubular fibrosis, and α-smooth muscle actin expression. However, inhibition of ERK1/2 activation led to significant compensatory upregulation of the MAP kinases, p38 and JNK in kidney tissue. CI-1040 also increased the expression of plasminogen activator inhibitor-1 (PAI-1), a key inhibitor of plasmin-dependent matrix metalloproteinases. Thus inhibition of ERK1/2 activation has no therapeutic effect on kidney fibrosis in SNx possibly due to increased compensatory activation of the p38 and JNK signalling pathways with subsequent upregulation of PAI-1
Inflammatory cytokines and biofilm production sustain Staphylococcus aureus outgrowth and persistence: A pivotal interplay in the pathogenesis of Atopic Dermatitis
Individuals with Atopic dermatitis (AD) are highly susceptible to Staphylococcus aureus colonization. However, the mechanisms driving this process as well as the impact of S. aureus in AD pathogenesis are still incompletely understood. In this study, we analysed the role of biofilm in sustaining S. aureus chronic persistence and its impact on AD severity. Further we explored whether key inflammatory cytokines overexpressed in AD might provide a selective advantage to S. aureus. Results show that the strength of biofilm production by S. aureus correlated with the severity of the skin lesion, being significantly higher (P < 0.01) in patients with a more severe form of the disease as compared to those individuals with mild AD. Additionally, interleukin (IL)-β and interferon γ (IFN-γ), but not interleukin (IL)-6, induced a concentration-dependent increase of S. aureus growth. This effect was not observed with coagulase-negative staphylococci isolated from the skin of AD patients. These findings indicate that inflammatory cytokines such as IL1-β and IFN-γ, can selectively promote S. aureus outgrowth, thus subverting the composition of the healthy skin microbiome. Moreover, biofilm production by S. aureus plays a relevant role in further supporting chronic colonization and disease severity, while providing an increased tolerance to antimicrobials
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