Abstract: A passive radiometric imaging device and a corresponding method for scanning a scene and reconstructing an image of said scene provide an improved image quality. The device comprises a radiometer for detecting radiation and a processing means for subsequently determining pixel values of pixels of the image to be reconstructed. A cost calculation unit calculates costs for the radiation samples of said data sub-set according to a predetermined cost function, said costs indicating the level of noise in the respective radiation sample. An optimization unit determines a pixel value as a label value from a set of label values, a label indicating a radiation sample or a group of radiation samples of the respective data sub-set, by determining an extremum of energy values determined for different radiation samples or different groups of radiation samples of the respective data sub-set by use of an energy function.

Abstract: An imaging device that segments a data set into one or more data sub-sets, each data sub-set comprising a plurality of measurement values of one or more neighboring spots; determines, per pixel, costs for the measurement values acquired at a position corresponding to a position of the pixel determines a pixel value for a pixel by determining a label value from a set of label values; and selects the measurement value at the spot indicated by the determined label as the pixel value.

Abstract: An indirect radar holography apparatus for scanning a scene and generating a high-density signal pattern representing the scene. The apparatus illuminates the scene with radiation according to an illumination signal; generates a reference signal from the illumination signal; detects radiation emitted in a predetermined spectral range from a spot of the scene; generates a radiation signal per spot from the detected radiation; performs control so that radiation is detected at a number of spots distributed over the scene, the number being lower than the number of intensity signals of the high-density signal pattern; combines the radiation signals generated from the detected radiation and the reference signals to obtain a low-density signal pattern of intensity signals; and processes the intensity signals of said low-density signal pattern to generate the high-density signal pattern by applying compressive sensing to the low-density signal pattern.

Abstract: A radar tomography apparatus and method determines one or more material properties of an object at a first number of positions distributed within a region of interest of said object. The apparatus includes one or more transmitters that transmit radiation, in particular microwave radiation, in the direction of the region of interest of the object, a plurality of receivers that receive radiation reflected from or transmitted through the region of interest of the object, a processor that processes the received radiation, said processor including a forward solver that determines electromagnetic field values at a second number of positions distributed in the region of interest from the received radiation.

Abstract: The present invention relates to a passive radiometric imaging device and a corresponding method for scanning a scene and reconstructing an image of said scene. To provide an improved image quality, the proposed device comprises a radiometer configured to detect radiation emitted in a predetermined spectral range from a plurality of spots of said scene to obtain a data set of radiation samples including at least one radiation sample per spot, and a processor configured to subsequently determine pixel values of pixels of the image to be reconstructed, said processor being configured to determine a pixel value of one of said pixels from a data sub-set of radiation samples from said data set, said data sub-set including the radiation samples detected at the spot corresponding to or being closest to the pixel, whose pixel value is to be determined, and/or radiation samples detected at neighboring spots.

Abstract: A passive radiometric imaging device and a corresponding method for scanning a scene and reconstructing an image of said scene provide an improved image quality. The device comprises a radiometer for detecting radiation and a processing means for subsequently determining pixel values of pixels of the image to be reconstructed. A cost calculation unit calculates costs for the radiation samples of said data sub-set according to a predetermined cost function, said costs indicating the level of noise in the respective radiation sample. An optimization unit determines a pixel value as a label value from a set of label values, a label indicating a radiation sample or a group of radiation samples of the respective data sub-set, by determining an extremum of energy values determined for different radiation samples or different groups of radiation samples of the respective data sub-set by use of an energy function.

Abstract: The present invention relates to a radar tomography apparatus and method for determining one or more material properties of an object at a first number of positions distributed within a region of interest of said object.

Abstract: The present invention relates to an indirect radar holography apparatus for scanning a scene and generating a high-density signal pattern representing said scene.

Abstract: The present invention relates to a passive radiometric imaging device and a corresponding method for scanning a scene and reconstructing an image of said scene. To provide an improved image quality, the proposed device comprises a radiometer configured to detect radiation emitted in a predetermined spectral range from a plurality of spots of said scene to obtain a data set of radiation samples including at least one radiation sample per spot, and a processor configured to subsequently determine pixel values of pixels of the image to be reconstructed, said processor being configured to determine a pixel value of one of said pixels from a data sub-set of radiation samples from said data set, said data sub-set including the radiation samples detected at the spot corresponding to or being closest to the pixel, whose pixel value is to be determined, and/or radiation samples detected at neighboring spots.

Abstract: We have recently identified (a) ectocalreticulin as the main source of immunogenicity of cancer cell death induced by chemotherapy or radiotherapy, (b) ectoERP57 as critical protein for inducing cell surface exposure of calreticulin, and (c) that ectoERP57 and ectocalreticulin are cotranslocated together to the tumor cell surface by the mediator of the inhibition of PP1/GADD34 complex. Here, I show the design of a peptide that inhibits the interaction between PP1 and GADD34 complex.

Abstract: A kit for treating a health condition in a mammal comprises a calreticulin protein and/or compound for inducing a translocation of a calreticulin protein to a cellular membrane in order to provoke an immunogenic apoptosis. The calreticulin protein may include any one or more of: endogenous calreticulin, recombinant calreticulin, and calreticulin in mimetic form. The endogenous form of calreticulin may include any one of: a plasma membrane calreticulin and an intracellular calreticulin.

Abstract: Anthracyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of calreticulin (CRT) and/or ERP57 to the cell surface. Knock down of CRT and/or ERP57 suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclines-induced CRT and/or ERP57 translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant colreticulin, and not recombinant ERP57, or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo.

Abstract: Anthracyclin-treated turn or cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclins induce the rapid, pre-apoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knock down of CRT suppressed the phagocytosis of anthracyclin-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclin-induced CRT translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy.

Abstract: Anthracyclines induce the rapid, pre-apoptotic translocation of ERP57 to the cell surface. Knock down of ERP57 inhibit the translocation of CRT, suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. In contrast, the blockade of ERP57 with blocking antibody had no effect on phagocytosis of anthracyclines-treated tumor cells by dendritic cells and their immunogenicity in mammals, such as mice. The anthracyclines-induced ERP57 translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant ERP57 did not restored the immunogenicity of cell death elicited by etoposide and mitomycin C, or enhanced their antitumor effects in vivo in contrast to the administration of recombinant CRT. These data identify the presence of ERP57 crucial for the translocation of CRT and to induce immunogenic cell death which will activate a anti-cancer immune responses.

Abstract: A screening method for testing the immunogenicity of new molecules and compounds and for testing fertility and sterility conditions. The method includes inducing a translocation of a calreticulin protein and/or an ERP57 protein, to a cellular membrane in order to determine the immunogenicity of the new molecules and compounds, or the fertility or sterility conditions. The method includes also the using of recombinant CRT and/or ERP57 to treat sterility.

Abstract: Anthrocyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of ERP57 to the cell surface. Knock down of ERP57 inhibit the translocation of CRT, suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. In contrast, the blockade of ERP57 with blocking antibody had no effect on phagocytosis of anthracyclines-treated tumor cells by dendritic cells and their immunogenicity in mammals, such as mice. The anthracyclines-induced ERP57 translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex.

Abstract: A pharmaceutical compound is used in the treatment of a health condition in a mammal. The compound comprises an antibody that interferes with an increased translocation of a protein, leading to an increased immunogenicity of cell death. The antibody may be, for example, anti-calreticulin and/or anti-ERP57. This antibody includes any one or more of blocking or neutralizing antibody.

Abstract: Anthracyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knock down of CRT suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclines-induced CRT translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy.

Abstract: A kit for treating a health condition in a mammal, comprises a ERP57 protein and/or compound for inducing a translocation of an ERP57 protein to a cellular membrane in order to provoke an immunogenic apoptosis. The ERP57 protein may include any one or more of: endogenous ERP57, recombinant ERP57, and ERP57 in mimetic form. The endogenous form of ERP57 may include any one of: a plasma membrane ERP57 and an intracellular ERP57.

Abstract: Anthracyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knock down of CRT suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclines-induced CRT translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy.