Weighted contrast enhancement based enhancement for remote sensing images

This paper discuss a novel approach based on dominant brightness level analysis and adaptive intensity transformation to enhance the contrast for remote sensing images. In this approach  we first perform discrete wavelet (DWT) on the input images and then decompose the bLL sub band into low-, middle-, and high-intensity layers using the log-average luminance. After estimating the intensity transformation, the resulting enhanced image is obtained by using the inverse DWT. The proposed algorithm overcomes this problem using the adaptive intensity transfer function. The experimental results show that the proposed algorithm enhances the overall contrast and visibility of local details better than existing techniques

Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells

20-HETE, the product of 20-hydroxylation of arachidonic acid by cytochrome P450 isoforms (CYP4F2 and CYP4A11), has a role in the oncogenesis of several human tumors. Recently, the GPR75 receptor has been identified as the target for 20-HETE. We have shown that androgen independent prostate cancer cells (PC-3) express GPR75. The aim of this study was to identify intracellular signaling molecules activated upon GPR75 stimulation by 20-HETE in PC-3 cells.Cells were incubated with 20-HETE (0.1 nM) in the presence or absence of the antagonist of the 20-HETE receptor, AAA (5 or 10 uM). Protein expression of the inducible focal adhesion protein Hydrogen Peroxide Inducible Clone-5 (HIC-5), the phosphorylated and total form of NF-kB, AKT, p38 MAP-Kinase (p38) and EGFR were assessed by western blot. Intracellular localization of p-AKT, NF-kB and PKCa were determined by immunofluorescence and subcellular fractionation. Migration of PC-3 cells incubated with diferentes inhibitors were evaluated by scratch wound healing assay. Results were analyzed using one-way ANOVA followed by Dunnet?s.Incubation with 20-HETE (2 h) increased the phosphorylation of EGFR, NF-kB and AKT by 146, 172 and 219%, respectively (vs control, p<0.01 for NF-kB, and p<0.001 for EGFR and AKT, n=3), and this was inhibited by AAA (vs 20-HETE alone, p<0.05 for NF-kB, p<0.01 for AKT and p<0.001 for EGFR). AAA alone increased p-38 phosphorylation by 248% (p<0.001 vs control, n=3). 20-HETE (1 h) induced the translocation of p-AKT to the nuclei (p<0.001, n=3) and promoted the redistribution of PKCa out of the nuclei (p<0.05, n=3) to the plasma membrane (p<0.001). Both effects were inhibited by AAA (vs 20-HETE, p<0.01 for AKT and p<0.05 for PKCa). AAA alone reduced the nuclear signal of p-AKT and NF-kB usually activated in tumoral cells (p<0.001 for both, n=3). Additionally, 20-HETE (12 h) increased by 150% the protein expression of Hic-5 (p<0.0001, n=5) and this was abolished by AAA (p<0.001).Our results show that 20-HETE modulates signaling pathways known to be deregulated in malignant cells through the GPR75-axis.Fil: Cardenas, Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Colombero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Dakarapu, Rambabu. University of Texas. Southwestern Medical Center; Estados UnidosFil: Falck, John. University of Texas. Southwestern Medical Center; Estados UnidosFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Nowicki, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaReunión anual de las Sociedades de BiocienciaMar del PlataArgentinaSociedad Argentina de Investigación ClínicaAsociación Argentina de Farmacología ExperimentalSociedad Argentina de BiologíaAsociación Argentina de Ciencia y Tecnología de Animales de LaboratorioSociedad Argentina de Protozoologí

Carbonylation of Csp3−H Bonds through Oxidative Wittig‐Type Reaction: An Unprecedented Version of Wittig Reaction

A Wittig‐type reaction was achieved by radical cation salt induced aerobic oxidation of Csp3−H bonds. Different from the “standard” version of the Wittig reaction, in which a carbon‐carbon double bond is formed from a carbonyl, carbonyl groups can be installed by similar process.Not from carbonyls but to carbonyls: A Wittig‐type reaction was achieved by radical cation salt induced aerobic oxidation of sp3 C−H bonds. Different from the “standard” version of the Wittig reaction, in which a carbon‐carbon double bond is formed from a carbonyl, carbonyl groups can be installed by similar process.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137437/1/ajoc201600055-sup-0001-misc_information.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137437/2/ajoc201600055.pd

Stereospecific Stille Cross-Couplings Using Mn(II)Cl₂

Cross-coupling reactions are a staple in organic synthesis, especially for C–C bond formation with sp- and sp²-carbon electrophiles. In recent years, the range of accessible C–C bonds has been extended to stereogenic centers which expedites access to greater molecular complexity. However, these reactions predominantly depend upon late transition metal (LTM) catalysts whose cost, toxicity, and/or environmental impact have come under increasing scrutiny and governmental regulation. Here, we report Mn­(II)­Cl₂ complexes alone, or with assistance from copper, catalyze the stereospecific cross-coupling of α-alkoxyalkylstannanes with organic electrophiles with complete retention of configuration

20-Hydroxyeicosatetraenoic acid (20-hete) promotes a malignant phenotype in human castration-resistant prostate cancer cells through stimulation of the g protein-coupled receptor gpr75

20-Hydroxyeicosatetraenoic acid (20- HETE), the product of 20-hydroxylation of arachidonic acid by cytochrome P450 isoforms (CYP4F2 and CYP4A11), has a role in the oncogenesis of several human tumors. Recently, the GPR75 receptor has been identified as the target for 20-HETE. We have shown that androgen independent prostate cancer cells (PC-3) express GPR75. The aim of this study was to assess in vitro if 20-HETE/GPR75 modify the metastatic features of PC-3 cells. Cells were incubated with 20-HETE or its stable analog 5,14- HEDGE (both 0.1 nM) in the presence or absence of two different antagonists of the 20-HETE receptor, AAA or 19-HEDE (both 5 or 10 uM). The following assays were performed: e-cadherin and vimentin protein expression (epithelial-mesenchymal transition), zymography (release of matrix metalloproteinase-2 (MMP-2)), immunofluorescence and p-FAK (changes of cytoskeleton), scratch wound healing (migration), and soft agar colony formation (anchorage-independent growth). Results were analyzed using one-way ANOVA followed by Dunnet’s. 20-HETE (24 h) increased by 150 % the expression of vimentin (p<0.0001, n= 3) and diminished by 40 % the expression of ecadherin (p<0.0001, n= 3), whereas these effects were reversed by AAA (p<0.0001 and p<0.05, respectively). 20-HETE increased by 52 % the release of MMP-2 (p<0.05, n= 3), and this was also inhibited by AAA (p<0.001). AAA disorganized the actin filaments throughout PC-3 cells, while tubulin filaments remained unchanged. Also, 20-HETE increased by 89 % FAK phosphorylation (Y397) (p<0.0001, n= 3). 20-HETE increased by 147 % cell migration rate (p<0.0001, n= 3) and this effect was reverted by both antagonists, AAA or 19-HEDE (p<0.05 and p<0.0001, respectively), or by knockdown of GPR75 (p<0.0001). Finally, 5,14-HEDGE (21 days) formed twice the number of colonies vs. control (p<0.05, n= 2) and this was abolished by AAA (p<0.05). These results strongly suggest a role for GPR75 in 20-HETE-mediated metastatic features in PC-3 cells.Fil: Cardenas, Sofia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Colombero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Panello, Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Dakarapu, Rambabu. University of Texas. Southwestern Medical Center; Estados UnidosFil: Falck, John. University of Texas. Southwestern Medical Center; Estados UnidosFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Nowicki, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaLXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); LI Reunión Anual de la Asociación Argentina de Farmacología Experimental (SAFE); XXI Reunión Anual de la Sociedad Argentina de Biología (SAB); XXXI Reunión Anual de la Sociedad Argentina de Protozoología (SAP) y IX Reunión Anual de la Asociación Argentina de Nanomedicinas (NANOMED-ar)Mar del PlataArgentinaSociedad Argentina de Investigación ClínicaAsociación Argentina de Farmacología ExperimentalSociedad Argentina de BiologíaSociedad Argentina de ProtozoologíaAsociación Argentina de Ciencia y Tecnología de Animales de LaboratorioAsociación Argentina de Nanomedicina

20-Hydroxyeicosatetraenoic acid (20- hete) promotes a malignant phenotype in human castration-resistant prostatecancer cells through stimulation of the g protein-coupled receptor GPR75

20-Hydroxyeicosatetraenoic acid (20- HETE), the product of 20-hydroxylation of arachidonic acid by cytochrome P450 isoforms (CYP4F2 and CYP4A11), has a role in the oncogenesis of several human tumors. Recently, the GPR75 receptor has been identified as the target for 20-HETE. We have shown that androgen independent prostate cancer cells (PC-3) express GPR75. The aim of this study was to assess in vitro if 20-HETE/GPR75 modify the metastatic features of PC-3 cells. Cells were incubated with 20-HETE or its stable analog 5,14- HEDGE (both 0.1 nM) in the presence or absence of two different antagonists of the 20-HETE receptor, AAA or 19-HEDE (both 5 or 10 uM). The following assays were performed: e-cadherin and vimentin protein expression (epithelial-mesenchymal transition), zymography (release of matrix metalloproteinase-2 (MMP-2)), immunofluorescence and p-FAK (changes of cytoskeleton), scratch wound healing (migration), and soft agar colony formation (anchorage-independent growth). Results were analyzed using one-way ANOVA followed by Dunnet’s. 20-HETE (24 h) increased by 150 % the expression of vimentin (p<0.0001, n= 3) and diminished by 40 % the expression of ecadherin (p<0.0001, n= 3), whereas these effects were reversed by AAA (p<0.0001 and p<0.05, respectively). 20-HETE increased by 52 % the release of MMP-2 (p<0.05, n= 3), and this was also inhibited by AAA (p<0.001). AAA disorganized the actin filaments throughout PC-3 cells, while tubulin filaments remained unchanged. Also, 20-HETE increased by 89 % FAK phosphorylation (Y397) (p<0.0001, n= 3). 20-HETE increased by 147 % cell migration rate (p<0.0001, n= 3) and this effect was reverted by both antagonists, AAA or 19-HEDE (p<0.05 and p<0.0001, respectively), or by knockdown of GPR75 (p<0.0001). Finally, 5,14-HEDGE (21 days) formed twice the number of colonies vs. control (p<0.05, n= 2) and this was abolished by AAA (p<0.05). These results strongly suggest a role for GPR75 in 20-HETE-mediated metastatic features in PC-3 cells.Fil: Cárdenas, Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Colombero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Dakarapu, Rambabu. University of Texas. Southwestern Medical Center; Estados UnidosFil: Falck, John. University of Texas. Southwestern Medical Center; Estados UnidosFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Nowicki, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaReunión Anual de las Sociedades de BiocienciaMar Del PlataArgentinaSociedad Argentina de Investigación ClinicaAsociación Argentina de Farmacología ExperimentalSociedad Argentina de BiologíaAsociación Argentina de Ciencia y Tecnología de Animales de LaboratorioSociedad Argentina de Protozoologí

Novel Roles of Epoxyeicosanoids in Regulating Cardiac Mitochondria

<div><p>Maintenance of a healthy pool of mitochondria is important for the function and survival of terminally differentiated cells such as cardiomyocytes. Epoxyeicosatrienoic acids (EETs) are epoxy lipids derived from metabolism of arachidonic acid by cytochrome P450 epoxygenases. We have previously shown that EETs trigger a protective response limiting mitochondrial dysfunction and reducing cellular death. The aim of this study was to investigate whether EET-mediated effects influence mitochondrial quality in HL-1 cardiac cells during starvation. HL-1 cells were subjected to serum- and amino acid free conditions for 24h. We employed a dual-acting synthetic analog UA-8 (13-(3-propylureido)tridec-8-enoic acid), possessing both EET-mimetic and soluble epoxide hydrolase (sEH) inhibitory properties, or 14,15-EET as model EET molecules. We demonstrated that EET-mediated events significantly improved mitochondrial function as assessed by preservation of the ADP/ATP ratio and oxidative respiratory capacity. Starvation induced mitochondrial hyperfusion observed in control cells was attenuated by UA-8. However, EET-mediated events did not affect the expression of mitochondrial dynamic proteins Fis1, DRP-1 or Mfn2. Rather we observed increased levels of OPA-1 oligomers and increased mitochondrial cristae density, which correlated with the preserved mitochondrial function. Increased DNA binding activity of pCREB and Nrf1/2 and increased SIRT1 activity together with elevated mitochondrial proteins suggest EET-mediated events led to preserved mitobiogenesis. Thus, we provide new evidence for EET-mediated events that preserve a healthier pool of mitochondria in cardiac cells following starvation-induced stress.</p></div

Morphometric analysis of mitochondrial dynamics.

<p><b>A.</b> 3D images of mitochondria were analyzed morphometrically to identify mitochondrial structures and to numerically report their length and size. Mitochondria were stained with MitoTracker Red (100nM) and Z-stacks images were captured with Zeiss AxioObserver Epifluorescence microscope. Image processing was conducted by Zeiss ZEN 12 and Bitplane Imaris software as detailed in the methods section. <b>B.</b> Distribution of mitochondria according to their length into long (>5μm), short (<5μm) and fragmented (<0.5μM) mitochondria. To verify the morphometric method in our cells, DRP1-dependent fission was inhibited by forskolin (20μM) and cyclosporine A (10μM) or activated by H89 (1μM) and iononmycin (5μM). <b>C.</b> The ratio of long mitochondria to short and fragmented mitochondria provides a single descriptor to mitochondrial length allowing simple statistical analysis between treatment groups. Values represent mean+SEM; <i>N</i> = 3 independent experiments, *, <i>p<</i>0.05 in comparison to control.</p

GPR75 receptor mediates 20-HETE-signaling and metastatic features of androgen-insensitive prostate cancer cells

Purpose: Recent studies have shown that 20-hydroxyeicosatetraenoic acid (20-HETE) is a key molecule in sustaining androgen-mediated prostate cancer cell survival. Thus, the aim of this study was to determine whether 20-HETE can affect the metastatic potential of androgen-insensitive prostate cancer cells, and the implication of the newly described 20-HETE receptor, GPR75, in mediating these effects. Methods: The expression of GPR75, protein phosphorylation, actin polymerization and protein distribution were assessed by western blot and/or fluorescence microscopy. Additionally, in vitro assays including epithelial-mesenchymal transition (EMT), metalloproteinase-2 (MMP-2) activity, scratch wound healing, transwell invasion and soft agar colony formation were used to evaluate the effects of 20-HETE agonists/antagonists or GPR75 gene silencing on the aggressive features of PC-3 cells. Results: 20-HETE (0.1 nM) promoted the acquisition of a mesenchymal phenotype by increasing EMT, the release of MMP-2, cell migration and invasion, actin stress fiber formation and anchorage-independent growth. Also, 20-HETE augmented the expression of HIC-5, the phosphorylation of EGFR, NF-κB, AKT and p-38 and the intracellular redistribution of p-AKT and PKCα. These effects were impaired by GPR75 antagonism and/or silencing. Accordingly, the inhibition of 20-HETE formation with N-hydroxy-N′-(4-n-butyl-2-methylphenyl) formamidine (HET0016) elicited the opposite effects. Conclusions: The present results show for the first time the involvement of the 20-HETE-GPR75 receptor in the activation of intracellular signaling known to be stimulated in cell malignant transformations leading to the differentiation of PC-3 cells towards a more aggressive phenotype. Targeting the 20-HETE/GPR75 pathway is a promising and novel approach to interfere with prostate tumor cell malignant progression.Fil: Cardenas Alcoser, Elena Sofia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Colombero Rivas, Cecilia Edith. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Dakarapu, Rambabu. University of Texas Southwestern Medical Center; Estados UnidosFil: Falck, John R.. University of Texas Southwestern Medical Center; Estados UnidosFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Nowicki, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; Argentin