Public attitudes toward forest management practices on pulp and paper company-owned forest lands in the southern Appalachian Region

Twenty-three community organizations participated in an educational program that addressed forest management practices on pulp and paper company-owned forest lands (for clarification, pulp and paper companies will be referred to as forest industry) in the Southern Appalachian Region. Initial attitudes were assessed using a pre-program questionnaire that focused on forest management practices on industry-owned land in the Southern Appalachian Region. An educational program was presented that addressed clearcutting, pine management, and erosion and sedimentation. The same questionnaire was then administered to identify any attitude changes that could be attributed to the educational program. This program was presented to several group-types which included church, civic, environmental, and professional groups in Asheville, North Carolina, Chattanooga, Tennessee, and Knoxville, Tennessee. The results suggest that the study population had generally supportive attitudes about industry. The educational program produced significant changes in attitudes in that respondents were more supportive in general. Finally, the attitudes of environmental groups changed most noticeably from non-supportive to generally supportive of industries current management practices

Genomic loss of tumor suppressor miRNA-204 promotes cancer cell migration and invasion by activating AKT/mTOR/Rac1 signaling and actin reorganization

Increasing evidence suggests that chromosomal regions containing microRNAs are functionally important in cancers. Here, we show that genomic loci encoding miR-204 are frequently lost in multiple cancers, including ovarian cancers, pediatric renal tumors, and breast cancers. MiR-204 shows drastically reduced expression in several cancers and acts as a potent tumor suppressor, inhibiting tumor metastasis in vivo when systemically delivered. We demonstrated that miR-204 exerts its function by targeting genes involved in tumorigenesis including brain-derived neurotrophic factor (BDNF), a neurotrophin family member which is known to promote tumor angiogenesis and invasiveness. Analysis of primary tumors shows that increased expression of BDNF or its receptor tropomyosin-related kinase B (TrkB) parallel a markedly reduced expression of miR-204. Our results reveal that loss of miR-204 results in BDNF overexpression and subsequent activation of the small GTPase Rac1 and actin reorganization through the AKT/mTOR signaling pathway leading to cancer cell migration and invasion. These results suggest that microdeletion of genomic loci containing miR-204 is directly linked with the deregulation of key oncogenic pathways that provide crucial stimulus for tumor growth and metastasis. Our findings provide a strong rationale for manipulating miR-204 levels therapeutically to suppress tumor metastasis

Recrutement de Palestiniennes en Israël, patriarcat et mouvements de femmes en Palestine

[…] – Comment l’occupation militaire israélienne perpétue-t-elle le patriarcat dans la société palestinienne ? – […] De nombreuses études ont montré que l’occupation israélienne actuelle est un élément clé de ce maintien du patriarcat dans la société palestinienne. L’occupation israélienne a anéanti le droit des Palestiniens à l’autodétermination, et a ainsi empêché le développement d’une constitution ou d’institutions légales en Palestine. En l’absence d’institutions légales autochtones, les..

Genomic Loss of Tumor Suppressor miRNA-204 Promotes Cancer Cell Migration and Invasion by Activating AKT/mTOR/Rac1 Signaling and Actin Reorganization

<div><p>Increasing evidence suggests that chromosomal regions containing microRNAs are functionally important in cancers. Here, we show that genomic loci encoding miR-204 are frequently lost in multiple cancers, including ovarian cancers, pediatric renal tumors, and breast cancers. MiR-204 shows drastically reduced expression in several cancers and acts as a potent tumor suppressor, inhibiting tumor metastasis in vivo when systemically delivered. We demonstrated that miR-204 exerts its function by targeting genes involved in tumorigenesis including <em>brain-derived neurotrophic factor</em> (<em>BDNF</em>), a neurotrophin family member which is known to promote tumor angiogenesis and invasiveness. Analysis of primary tumors shows that increased expression of BDNF or its receptor tropomyosin-related kinase B (TrkB) parallel a markedly reduced expression of miR-204. Our results reveal that loss of miR-204 results in BDNF overexpression and subsequent activation of the small GTPase Rac1 and actin reorganization through the AKT/mTOR signaling pathway leading to cancer cell migration and invasion. These results suggest that microdeletion of genomic loci containing miR-204 is directly linked with the deregulation of key oncogenic pathways that provide crucial stimulus for tumor growth and metastasis. Our findings provide a strong rationale for manipulating miR-204 levels therapeutically to suppress tumor metastasis.</p> </div

Vorinostat increases CFTR band B and augments ion channel activity in combination with lumacaftor.

<p>(A) Western blot of cell lysates treated with vorinostat from HeLa (left panel) or HEK 293 (right panel) cells. (B) Short circuit current measurements in CFBE monolayers treated with vorinostat, lumacaftor or a combination of the two compounds. After establishment of a Cl^- gradient and addition of amiloride (100 μM), monolayers were treated with forskolin (20 μM) and ivacaftor (VX-770, 10 μM), followed by administration of CFTR Inhibitor 172 (10 μM). N = 4 filters per condition. Error bars represent SEM with p values indicated.</p

Cellular processes that influence the F508del CFTR pool.

<p>Cellular processes that influence the F508del CFTR pool.</p

Fluorescence based total cellular CFTR measurement.

<p>(A) Cartoon depicts fluorescence based analysis in the microtiter plate assay. (B) Examples of positive hits from a screen of ~10,000 compounds using libraries including Pharmakon-1600, Enamine_30K, Enzo_FDA_01, and Selleck_FDA_01. Each value shown is >3 standard deviations above mean for all compounds tested.</p

Computational chemistry as a means to identify improved E1 ubiquitin activating enzyme inhibitors.

<p>The PYR-41 binding site was modeled and suitability as a “druggable” target assessed by SiteMap [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0163615#pone.0163615.ref026" target="_blank">26</a>]. Features of the predicted binding site (insert) describe a molecular target appropriate for drug optimization. The right panel shows docking of PYR-41 to the E-1 activating enzyme.</p

Verification of the hits using western analysis and transepithelial conductance measurements.

<p>(A) Western blots of cell lysates from HeLa expressing F508del CFTR treated for 24 hours with 10 μM primary hit compounds identified to increase total CFTR fluorescence. (B) Transepithelial conductance measurements after 24 hours incubation with selected compounds alone (10 μM), or combined with lumacaftor (3 μM). (C) Chemical structure of vorinostat.</p