Growth of Carbon Nanotubes on Carbon Fiber by Thermal CVD Using Ni Nanoparticles as Catalysts

AbstractNickel nanoparticles and thin film on carbon fiber have been prepared through electroless deposition. Moreover, carbon nanotubes were grown on carbon fiber covered by nickel nanoparticles using thermal chemical vapor deposition. The effects of changes in the thickness of the nickel catalyst layer and the growth temperature of carbon nanotubes were studied systemically, and the results are discussed in the present work

Entangled Dilaton Dyons

Einstein-Maxwell theory coupled to a dilaton is known to give rise to extremal solutions with hyperscaling violation. We study the behaviour of these solutions in the presence of a small magnetic field. We find that in a region of parameter space the magnetic field is relevant in the infra-red and completely changes the behaviour of the solution which now flows to an $AdS_2\times R^2$ attractor. As a result there is an extensive ground state entropy and the entanglement entropy of a sufficiently big region on the boundary grows like the volume. In particular, this happens for values of parameters at which the purely electric theory has an entanglement entropy growing with the area, $A$, like $A \log(A)$ which is believed to be a characteristic feature of a Fermi surface. Some other thermodynamic properties are also analysed and a more detailed characterisation of the entanglement entropy is also carried out in the presence of a magnetic field. Other regions of parameter space not described by the $AdS_2\times R^2$ end point are also discussed.Comment: Some comments regarding comparison with weakly coupled Fermi liquid changed, typos corrected and caption of a figure modifie

Altered Retinoic Acid Metabolism in Diabetic Mouse Kidney Identified by 18O Isotopic Labeling and 2D Mass Spectrometry

Numerous metabolic pathways have been implicated in diabetes-induced renal injury, yet few studies have utilized unbiased systems biology approaches for mapping the interconnectivity of diabetes-dysregulated proteins that are involved. We utilized a global, quantitative, differential proteomic approach to identify a novel retinoic acid hub in renal cortical protein networks dysregulated by type 2 diabetes.Total proteins were extracted from renal cortex of control and db/db mice at 20 weeks of age (after 12 weeks of hyperglycemia in the diabetic mice). Following trypsinization, (18)O- and (16)O-labeled control and diabetic peptides, respectively, were pooled and separated by two dimensional liquid chromatography (strong cation exchange creating 60 fractions further separated by nano-HPLC), followed by peptide identification and quantification using mass spectrometry. Proteomic analysis identified 53 proteins with fold change >or=1.5 and p<or=0.05 after Benjamini-Hochberg adjustment (out of 1,806 proteins identified), including alcohol dehydrogenase (ADH) and retinaldehyde dehydrogenase (RALDH1/ALDH1A1). Ingenuity Pathway Analysis identified altered retinoic acid as a key signaling hub that was altered in the diabetic renal cortical proteome. Western blotting and real-time PCR confirmed diabetes-induced upregulation of RALDH1, which was localized by immunofluorescence predominantly to the proximal tubule in the diabetic renal cortex, while PCR confirmed the downregulation of ADH identified with mass spectrometry. Despite increased renal cortical tissue levels of retinol and RALDH1 in db/db versus control mice, all-trans-retinoic acid was significantly decreased in association with a significant decrease in PPARbeta/delta mRNA.Our results indicate that retinoic acid metabolism is significantly dysregulated in diabetic kidneys, and suggest that a shift in all-trans-retinoic acid metabolism is a novel feature in type 2 diabetic renal disease. Our observations provide novel insights into potential links between altered lipid metabolism and other gene networks controlled by retinoic acid in the diabetic kidney, and demonstrate the utility of using systems biology to gain new insights into diabetic nephropathy

Atypical Respiratory Distress in A Newborn: a Diagnostic Dilemma

Neonatal respiratory distress is a very common problem in our practice. The causes may be respiratory, cardiovascular, central, metabolic, haematological and surgical. The cause of distress due to transient myocardial depression is not very common in mild asphyxia. We present a case having transient myocardial depression with severe respiratory distress and features of shock in a mild asphyxiated baby

Granulocyte colony-stimulating factor partially repairs the damage provoked by Trypanosoma cruzi in murine myocardium

Background: The hallmark of Trypanosoma cruzi infection is cardiomyopathy that leads to end-stage heart failure. We investigated whether G-CSF, known to induce heart tissue repair by bone marrow stem cell mobilization,ameliorates T. cruzi-induced myocarditis. Methods and results: T. cruzi-infected C3H/He mice were treated with G-CSF and monitored for parasite burden,BMSC mobilization, cytokine profile and cardiac remodeling. G-CSF increased the expression of CXCR4, CD34, and c-Kit, indicatingmobilization and migration of BMSC, some of which differentiated to cardiomyocytes as evidenced by increased levels of GATA4+/MEF2C+ cells and desmin expression in chagasic hearts. G-CSF enhanced amixed cytokine response (IL-10 + TGF-β > IFN-γ + TNF-α > IL-4) associated with increased heart inflammation and no beneficial effect on parasite control. Further, G-CSF controlled T. cruzi-induced extracellular-matrix alterations of collagens (Col I and Col llI), hydroxyproline, and glycosaminoglycan contents and promoted compensatory cardiac remodeling; however, these responses were not sufficient to control T. cruzi-induced cardiomyocyte atrophy. Benznidazole treatment prior to G-CSF resulted in the control of parasitism and parasite-induced inflammation, and subsequently, G-CSF was effective in executing the tissue repair, as evidenced by extracellular-matrix homeostasis and normalization of cardiomyocyte size in chagasic hearts. Conclusions: G-CSF treatment after T. cruzi infection enhanced migration and homing of BMSC, some of which differentiated to cardiomyocytes. Yet, G-CSF promoted a mixed (Treg > Th1 > Th2) immune response that contributed to persistent inflammation and limited improvement in cardiac homeostasis. Combinatorial therapy (BZ → G-CSF) was beneficial in arresting inflammatory processes and tissue damage in chagasic hearts.Fil: González, Mariela Natacha. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; ArgentinaFil: Dey, Nilay. University of Texas Medical Branch. Departments of Microbiology and Immunology and Pathology; Estados UnidosFil: Garg, Nisha J.. University of Texas Medical Branch. Departments of Microbiology and Immunology and Pathology; Estados UnidosFil: Postan, Miriam. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Dirección Nacional de Instituto de Investigación. Administración Nacional de Laboratorio e Instituto de Salud. Instituto Nacional de Parasitología; Argentin

Internal Jugular Vein Phlebectasia Presenting with Hoarseness of Voice

Internal jugular phlebectasia presents as a soft cystic mass in the neck that appears on straining. We present a case of a 7-year-old girl who presented with a painless soft cystic mass in the neck associated with hoarseness of voice. Based on clinical examination and CT image, diagnosis of right internal jugular phlebectasia was made

Integrated Functional Analysis of the Nuclear Proteome of Classically and Alternatively Activated Macrophages

Macrophages (Mφ) play a central role in coordinating host response to pathogens, cellular injury, and environmental stimuli. Herein, we report multidimensional, nuclear proteomic analyses of protein expression and posttranslational modifications (PTMs) that control biological processes during Mφ activation. For this, Mφ were incubated with IFN-γ/LPS and IL-4, and their differentiation to proinflammatory (M1) and anti-inflammatory (M2a, referred as M2 for simplicity throughtout the manuscript) phenotypes was confirmed by detection of CD64 and CD206 surface markers and TNF-α, arginase I, and iNOS-dependent nitrite levels. We used a sequential method of organellar enrichment and labeling of nuclear fractions with BODIPY FL-maleimide fluorescence dye followed by two-dimensional electrophoresis (2DE) to capture quantitative changes in abundance and S-nitrosylated (SNO) proteome signatures. Exact same gels were then labeled with Pro-Q Diamond to detect protein phosphorylation. MALDI-TOF/TOF MS analysis of the protein spots with fold change of ≥1.5 in any of the groups yielded 229 identifications. We found that 145, 78, and 173 protein spots in M1 Mφ and 105, 81, and 164 protein spots in M2 Mφ were changed in abundance, S-nitrosylation, and phosphorylation, respectively, with respect to M0 controls (fold change: ≥1.5, p≤0.05). Targeted analysis by immunoprecipitation and Western blotting was performed to verify the differential abundance and phosphorylation levels of two of the proteins in M1 and M2 (vs. M0) Mφ. Ingenuity Pathway Analysis of the nuclear proteome datasets showed that the abundance and posttranslational (SNO and Phosphor) modifications of the proteins predicted to be involved in cytoskeletal organization/cell movement, phagocytosis/endocytosis, and cell proliferation/cell death were differentially regulated with proinflammatory and anti-inflammatory activation of Mφ

Liver inflammatory cytokine response to treatment with anti-parasite drugs.

<p>Liver tissues were harvested after ST and LT treatment with NFOH, BZL, and vehicle, as detailed in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0003231#pntd-0003231-g001" target="_blank">Fig. 1</a>. (<b>A</b>) Shown are the relative changes in gene expression for TNF-α, determined by real time RT-PCR. Results were normalized to GAPDH mRNA. (<b>B</b>) TNF-α levels in tissue homogenates were determined by an ELISA.</p