70 research outputs found

    Geostatistically estimation and mapping of forest stock in a natural unmanaged forest in the Caspian region of Iran

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    Estimation and mapping of forest resources are preconditions for management, planning and research. In this study, we applied kriging interpolation of geostatistics for estimation and mapping of forest stock at-tributes in a natural, uneven-aged, unmanaged forest in the Caspian region of northern Iran. The site of the study has an area of 516 ha and an elevation that ranges from 1100 to 1450 m a.s.l. Field sampling was per-formed on a 75m × 200m systematic grid using 309 geo-referenced circular sample plots of 1000 m2 area. Experimental variograms were calculated and plotted for basal area (BA), volume (V) and stem density (N). Whereas the calculated variograms of BA and V exhibited spatial auto-correlation only after data stratification based on diameter size classes and tree species, the variogram of stem density displayed a moderate spatial structure that was fitted by a spherical model. Stem density was estimated by ordinary block kriging and the accuracy of estimation was validated by cross-validation result. We conclude that geostatistical approaches have the potential to more accurately capture and describe the spatial variability of forest stock, and thus reduce the uncertainty in estimates of stem density as well as produce more accurate stem density maps of forests in comparison with the spatially uninformed classic method. Geostatistical methods provide a very suitable tool to derive more accurate estimates of growing stock, particularly in structurally complex, unmanaged, uneven-aged forest such as this one from the Caspian region of northern Iran

    Toll-Like Receptors 2, 4, and 9 Modulate Promoting Effect of COPD-Like Airway Inflammation on K-Ras-Driven Lung Cancer Through Activation of the MyD88/NF-ĸB Pathway in the Airway Epithelium

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    INTRODUCTION: Toll-like receptors (TLRs) are an extensive group of proteins involved in host defense processes that express themselves upon the increased production of endogenous damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) due to the constant contact that airway epithelium may have with pathogenic foreign antigens. We have previously shown that COPD-like airway inflammation induced by exposure to an aerosolized lysate of nontypeable METHODS: In the present study, we have dissected the role of TLRs in this process by knocking out TLR2, 4, and 9 and analyzing how these deletions affect the promoting effect of COPD-like airway inflammation on K-ras-driven lung adenocarcinoma. RESULTS: We found that knockout of TLR 2, 4, or 9 results in a lower tumor burden, reduced angiogenesis, and tumor cell proliferation, accompanied by increased tumor cell apoptosis and reprogramming of the tumor microenvironment to one that is antitumorigenic. Additionally, knocking out of downstream signaling pathways, MyD88/NF-κB in the airway epithelial cells further recapitulated this initial finding. DISCUSSION: Our study expands the current knowledge of the roles that TLR signaling plays in lung cancer, which we hope, can pave the way for more reliable and efficacious prevention and treatment modalities for lung cancer

    Conformational rearrangements in the transmembrane domain of CNGA1 channels revealed by single-molecule force spectroscopy

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    Cyclic nucleotide-gated (CNG) channels are activated by binding of cyclic nucleotides. Although structural studies have identified the channel pore and selectivity filter, conformation changes associated with gating remain poorly understood. Here we combine single-molecule force spectroscopy (SMFS) with mutagenesis, bioinformatics and electrophysiology to study conformational changes associated with gating. By expressing functional channels with SMFS fingerprints in Xenopus laevis oocytes, we were able to investigate gating of CNGA1 in a physiological-like membrane. Force spectra determined that the S4 transmembrane domain is mechanically coupled to S5 in the closed state, but S3 in the open state. We also show there are multiple pathways for the unfolding of the transmembrane domains, probably caused by a different degree of \u3b1-helix folding. This approach demonstrates that CNG transmembrane domains have dynamic structure and establishes SMFS as a tool for probing conformational change in ion channels

    Early phase of plasticity-related gene regulation and SRF dependent transcription in the hippocampus

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    Hippocampal organotypic cultures are a highly reliable in vitro model for studying neuroplasticity: in this paper, we analyze the early phase of the transcriptional response induced by a 20 \ub5M gabazine treatment (GabT), a GABA-Ar antagonist, by using Affymetrix oligonucleotide microarray, RT-PCR based time-course and chromatin-immuno-precipitation. The transcriptome profiling revealed that the pool of genes up-regulated by GabT, besides being strongly related to the regulation of growth and synaptic transmission, is also endowed with neuro-protective and pro-survival properties. By using RT-PCR, we quantified a time-course of the transient expression for 33 of the highest up-regulated genes, with an average sampling rate of 10 minutes and covering the time interval [10 3690] minutes. The cluster analysis of the time-course disclosed the existence of three different dynamical patterns, one of which proved, in a statistical analysis based on results from previous works, to be significantly related with SRF-dependent regulation (p-value<0.05). The chromatin immunoprecipitation (chip) assay confirmed the rich presence of working CArG boxes in the genes belonging to the latter dynamical pattern and therefore validated the statistical analysis. Furthermore, an in silico analysis of the promoters revealed the presence of additional conserved CArG boxes upstream of the genes Nr4a1 and Rgs2. The chip assay confirmed a significant SRF signal in the Nr4a1 CArG box but not in the Rgs2 CArG box

    Glaucoma, Stem Cells, and Gene Therapy: Where Are We Now?

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    Glaucoma is the second most common cause of blindness, affecting 70∼80 million people around the world. The death of retinal ganglion cells (RGCs) is the main cause of blindness related to this disease. Current therapies do not provide enough protection and regeneration of RGCs. A novel opportunity for treatment of glaucoma is application of technologies related to stem cell and gene therapy. In this perspective we will thus focus on emerging approaches to glaucoma treatment including stem cells and gene therapy
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