Use of remote sensing for determination of the water content

Using SAR data for wet snow monitoring Abstract This paper focuses on an existing method of snow information retrieval by means of satellite SAR data. The method was first presented by Malnes and Guneriussen (2002), and has been proven to be capable of sub-pixel classification of wet snow. It is also able to classify dry snow pixels. The classification is based on change detection, so a snow-free reference image is required. Some flaws in this algorithm have been discovered during the work on this paper and are discussed, as well as a possible solution is suggested. Because this method is uncapable of classifying pixels containing water bodies, I have proposed an algorithm that can classify snow cover on lakes to enhance its capabilities. Also, a way to improve the wet snow cover classification by means of optical data was suggested. Keywords: SAR, snow cover, remote sensing, wet sno

Additional file 7: Table S4. of Axitinib and sorafenib are potent in tyrosine kinase inhibitor resistant chronic myeloid leukemia cells

Anti-GAB2 IP of Imatinib, Axitinib and Sorafenib vs DMSO treated cells. SILAC ratios are normalized to GAB2. Only sites with localization probabilities greater 0.75 and Andromeda scores greater 40 are shown. PEP: posterior error probability. (XLSX 12 kb

Additional file 1: Figure S1. of Axitinib and sorafenib are potent in tyrosine kinase inhibitor resistant chronic myeloid leukemia cells

(A/B) Ba/F3 vector cells and cells transformed with pBABE Bcr-Abl were exposed to the indicated inhibitors or DMSO for 48 h. Cells were stained with 7-AAD and assessed for viability (A) or metabolic activity (MTT assay) (B). (C) KBM5 and KBM5-T315I cells were exposed to the indicated inhibitors or DMSO for 48 h. Cells were assessed for metabolic activity (MTT assay) (D/E) K562 cells overexpressing Lyn or hyperactive Lyn Y508F were exposed to the indicated inhibitors or DMSO for 48 h. Cells were stained with 7-AAD and assessed for viability (D) or metabolic activity (MTT assay) (E). Relevant statistically significant effects are indicated by asterisks, all statistical data can be found above. (PDF 176 kb

Additional file 2: Figure S2. of Axitinib and sorafenib are potent in tyrosine kinase inhibitor resistant chronic myeloid leukemia cells

(A/B) Western Blot quantification of Fig. 1d and 1G, n = 3, using FusionCapt 7.06 (Vilber Lourmat, Germany). (PDF 184 kb

The Smac mimetic SM83 sensitizes oncogenic K-Ras expressing CRC cells to Db_αEGFR-scTRAIL.

<p>(a–d) Caco-2tet Ras^G12V cells were seeded into 3D cultures in the presence of doxycycline. (a) Three days later, cultures were left untreated or treated with 5 µM SM83 or 20 µM Z-VAD for 1 h prior to addition of 1 nM Db_αEGFR-scTRAIL. Viability was measured 24 h later by MTT assay and normalized to the untreated control (n = 3). (b) 24 h after treatment, cells were fixed and stained for DNA strand breaks. Tunel-positive cells were counted (n = 2). (c) Three days post seeding, cultures were left untreated (ut) or treated with 5 µM SM83. Cells were recovered from the cultures 24 h later and lysates were analyzed by immunoblotting. Shown is one representative blot of two independent experiments. Tubulin was detected as a loading control. (d) Quantification of Western blots from (c). Protein levels were normalized to the corresponding tubulin control; levels in the untreated cultures were set as 1 (n = 2). (e, f) HCT-116 and LoVo cells were grown in 3D cultures for six days, and then fixed and stained for F-actin and DNA (DAPI) (scale bar: 20 µm) (top panels). Three days post seeding, cultures were left untreated or pretreated with 5 µM SM83 prior to addition of 0.05 nM Db_αEGFR-scTRAIL. Viability was measured 24 h later by MTT assay and normalized to the untreated control (bottom panels) (n = 3).</p

EGFR-directed targeting determines the bioactivity of Db_αEGFR-scTRAIL.

<p>(a) Caco-2 cells grown in 2D were left untreated or treated with 4 nM Db_αEGFR-scTRAIL or 4 nM Cetuximab for 15 min prior to stimulation with EGF or TGF-α (10 ng/ml) for 10 min. Phosphorylated and total proteins were detected by immunoblotting. Shown is one representative blot of three independent experiments. Tubulin was detected as a loading control. (b) Quantification of Western blots from (a). Phospho-EGFR levels were normalized to the corresponding total protein levels; levels in the untreated control were set as 1 (n = 3). (c, d). Three days post seeding, Caco-2 3D cultures grown in the absence or presence of growth factors were treated with 1 nM Db_αEGFR-scTRAIL. (c) Viability was determined by MTT assay after 72 h and normalized to the respective untreated control (ut). (n = 3) (d) Caspase 3/7 activity was measured after 24 h. Values were normalized to the corresponding untreated control (n = 3). (e) Three days post seeding, Caco-2 3D cultures were either left untreated or treated with 5 nM Db_αEGFR-scTRAIL for 72 h. Surviving cysts in the phase contrast images are indicated by arrows (scale bar: 50 µm). (f) Lysates derived from the 3D cultures shown in (e) were analyzed by immunoblotting. Shown is one representative blot of three independent experiments. Tubulin was detected as a loading control. Specific bands are marked by arrowheads. (g) Quantification of Western blots from (f). Protein levels were normalized to the corresponding tubulin control; levels in the untreated cultures were set as 1 (n = 3).</p

Caco-2 3D cultures are sensitive to Db_αEGFR-scTRAIL.

<p>Cells were grown in 3D or 2D in medium containing 10% FCS. (a) Three days post seeding, cultures were treated with Db_αEGFR-scTRAIL. Viability was measured 72 h later by MTT assay and normalized to the untreated control (n = 3). (b) Phase contrast images of the 3D and 2D cultures described in (a) treated with the indicated concentrations of Db_αEGFR-scTRAIL for 72 h (scale bar: 50 µm). (c) Three days post seeding, 3D cultures were pretreated with 20 µM Z-VAD as indicated before addition of 1 nM Db_αEGFR-scTRAIL. Viability was measured 72 h later by MTT assay and normalized to the untreated control (ut) (n = 3). (d) 24 h after treatment, cells were fixed and stained for DNA strand breaks. Tunel-positive cells were counted (n = 2). (e) Representative pictures of the Tunel stainings described in (d), Tunel-positive cells (red), DAPI (nuclei; blue). Shown are confocal sections (scale bar: 100 µm). (f) Three days post seeding, cultures were treated with 0.1 nM or 1 nM Db_αEGFR-scTRAIL for 24 h. Caspase 3/7 activity was measured and normalized to the respective untreated control (ut) (n = 3). (g) Four days post seeding, lysates were generated and analyzed by immunoblotting. Shown is one representative blot of three independent experiments. Tubulin was detected as a loading control. Specific bands are marked by arrowheads. (h) Quantification of Western blots from (g). Protein levels were normalized to the corresponding tubulin control; levels in the 2D cultures were set as 1 (n = 3).</p

Caco-2 3D cultures are sensitive to pharmacological EGFR inhibition.

<p>Caco-2 cells were grown in 3D cultures containing 2% FCS in the presence of growth factors (10 ng/ml) or in 2% FCS only (con). (a) Cultures were analyzed by MTT assay at day 6 and normalized to the control (n = 5). (b) Three days post seeding 100 ng/ml CTX was added to induce lumen expansion. Spheroids were fixed on day 6 and stained with phalloidin (F-actin) and DAPI (nuclei). Shown are confocal sections of a representative cyst (scale bar: 10 µm). (c) Three days after seeding, 3D cultures were left untreated or treated with 0.5 µM Cetuximab (Cet) for 72 h. Viability was determined by MTT assay and normalized to the untreated control (ut). (n = 4) (d) Caco-2 3D cultures were left untreated or treated with 0.5 µM Cetuximab for 72 h and analyzed by phase microscopy (scale bar: 50 µm). (e) Three days after seeding, 3D cultures were left untreated (ut) or treated with 0.5 µM Cetuximab (Cet) for 72 h. Cytotoxicity was determined using the CytoTox-Glo Cytotoxicity Assay (n = 3).</p

Inducible expression of oncogenic K-Ras^G12V in Caco-2tet cells.

<p>(a) Caco-2tet vector control and K-Ras^G12V cells were treated with 2 µg/ml doxycycline for 72 h (+dox). Cells were harvested and GFP fluorescence was analyzed by flow cytometry. Non-induced cells were used as a control (−dox). (b) Caco-2tet vector control and K-Ras^G12V cells were grown in 2D and treated with doxycycline for the indicated times prior to lysis. GFP, Ras, pERK (T202/Y204) and ERK levels were determined by Western blotting. Tubulin was detected as a loading control. All panels shown are from the same blot. (c) Caco-2tet vector control and K-Ras^G12V cells were seeded into 3D cultures in the absence or presence of doxycycline. Three days post seeding lumen expansion was induced by addition of 100 ng/ml CTX. Cultures were fixed three days later and stained with E-cadherin-specific antibody (green), phalloidin (red) and DAPI (nuclei; blue). Shown are confocal sections of representative cysts (scale bar: 10 µm).</p

Additional file 8: Figure S3. of MCL-1 inhibition provides a new way to suppress breast cancer metastasis and increase sensitivity to dasatinib

showing that MCL-1 antagonism by BIMs2A slows tumor growth in mice bearing MDA-MB-468-2A xenografts but not MDA-MB-231-2A xenografts. (A–F) Line graphs depicting the tumor growth curves of MDA-MB-468-2A xenografts (A, B) and MDA-MB-231-2A xenografts (C, D) from mice fed with DOX or control food. Linear regression of these curves shown in B and D respectively. A comparison of the growth rate of tumors in mice bearing MDA-MB-468-2A (black) and MDA-MB-231-2A (red) xenografts fed with control food (E, F). (JPG 1348 kb