Abstract: The present disclosure provides an optical coherent imager implemented on a photonic integrated circuit (PIC) that enables shared path for transmitting and receiving optical signals by exploiting polarization diversity. The present disclosure also provides an optical coherent imager including an array of the optical coherent sensing units to simplify the design and calibrations of the imager, and a method for coherent sensing by the optical coherent imager.

Abstract: A method for treating a subject suffering from refractory rheumatoid arthritis includes the step of administering an effective amount of a quinonemethide triterpenoid or a pharmaceutically tolerable salt, solvate or anhydrate thereof to the subject. Also is a method for inducing autophagy in a synovial fibroblast, and a method of inducing calcium mobilization in a synovial fibroblast. Further a pharmaceutical composition includes an effective dose of a quinonemethide triterpenoid and an anti-arthritis compound. The quinonemethide triterpenoid is suitable to treat refractory rheumatoid arthritis (RA) in particular ABC-protein-dependent RA and apoptosis-deficient RA. The quinonemethide triterpenoid also possesses significant inhibitory effects on the growth of synovial fibroblasts, in particular modulating the calcium homeostasis in multidrug-resistant rheumatoid arthritis synovial fibroblasts.

Abstract: A method for treating a subject suffering from a neurodegenerative disease includes administering at least one triterpenoid which can be obtained from Hedera helix. A method for treating a subject suffering from a neurodegenerative disease includes administering an effective amount of a Hedera helix extract which comprises the triterpenoid. The neurodegenerative disease is preferably but not exclusively Parkinson's disease or Huntington's disease. Methods for extracting the triterpenoid from Hedera helix and a method for inducing autophagy in cells by contacting them with the triterpenoid are also provided. The triterpenoid allows an exceptional induction of autophagy, in particular a significant reduction of the protein level of mutant huntingtin, a significant reduction of the protein level of A53T ?-synuclein, a significant inhibition of the oligomerization of ?-synuclein and a significant inhibition of the inclusion formation of huntingtin via the AMPK-mTOR dependent autophagy inducing pathway.

Abstract: A method for inhibiting the expression and/or functional activity of an ABC transporter protein in a subject suffering from a disorder associated with an overexpression of the ABC transporter protein includes administrating a cobalt-polypyridyl complex to the subject. A method for inhibiting the expression and/or functional activity of an ABC transporter in cells includes contacting the cells with an effective amount of the cobalt-polypyridyl complex.

Abstract: A quinonemethide triterpenoid is administered to subjects with multidrug-resistant cancer, in particular a cancer with enhanced expression and/or functional activity of ABC transporter proteins such as P-glycoprotein and/or an apoptosis-deficient, in particular p53-, Bax- or Bak-deficient, cancer, i.e. specific subgroups of subjects with cancer. The quinonemethide triterpenoid is suitable to treat cancer allowing for an accumulation of cytotoxic or therapeutic compounds in the cells while having exceptionally increased cytotoxic activity towards the multidrug-resistant cancer cells and while allowing for an increased activity of chemotherapeutic compounds. Methods for specifically targeting cancer cells with multidrug-resistance and methods for potentiating the activity of a chemotherapeutic compound in those cancer cells are also disclosed. A kit including a quinonemethide triterpenoid and a chemotherapeutic compound is also provided.

Abstract: A method for treating a subject suffering from refractory rheumatoid arthritis includes the step of administering an effective amount of a quinonemethide triterpenoid or a pharmaceutically tolerable salt, solvate or anhydrate thereof to the subject. Also is a method for inducing autophagy in a synovial fibroblast, and a method of inducing calcium mobilization in a synovial fibroblast. Further a pharmaceutical composition includes an effective dose of a quinonemethide triterpenoid and an anti-arthritis compound. The quinonemethide triterpenoid is suitable to treat refractory rheumatoid arthritis (RA) in particular ABC-protein-dependent RA and apoptosis-deficient RA. The quinonemethide triterpenoid also possesses significant inhibitory effects on the growth of synovial fibroblasts, in particular modulating the calcium homeostasis in multidrug-resistant rheumatoid arthritis synovial fibroblasts.

Abstract: Prenylated isoflavones are suitable to specifically inhibit P-glycoprotein in multidrug-resistant cancer cells leading to an accumulation of cytotoxic compounds or therapeutic compounds in the cells while having exceptionally increased cytotoxic activity specifically towards multidrug-resistant cancer cells and while allowing for an increased activity of chemotherapeutic compounds towards which the cells are resistant. Also in accordance with the present invention is a method for specifically targeting cancer cells with multidrug-resistance as well as a method of potentiating the activity of a chemotherapeutic compound in multidrug-resistant cancer cells. In a further aspect, a kit including a prenylated isoflavone and a chemotherapeutic compound is provided.

Abstract: The present invention provides an in vivo platform for identifying and determining therapeutic or prophylactic activity of test compounds in delay-type hypersensitivity (DTH) and other inflammatory or cancerous diseases mediated by activation of IKK-?C46A mutants. The in vivo platform of the present invention is a non-human transgenic mammal, e.g., a mouse model, with a site directed mutagenesis at a cysteine residue replaced by alanine in IKK-? protein kinase. The site directed mutagenesis is introduced by a specially designed targeting vector containing a transversion in exon 3 of the Ikbkb genes encoding the IKK-?. The present invention also provides methods for generating the transgenic mammal and for determining and identifying compounds that can inhibit activation of IKK-?C46A mutants.

Abstract: A method for treating a subject suffering from a neurodegenerative disease includes administering at least one triterpenoid which can be obtained from Hedera helix. A method for treating a subject suffering from a neurodegenerative disease includes administering an effective amount of a Hedera helix extract which comprises the triterpenoid. The neurodegenerative disease is preferably but not exclusively Parkinson's disease or Huntington's disease. Methods for extracting the triterpenoid from Hedera helix and a method for inducing autophagy in cells by contacting them with the triterpenoid are also provided. The triterpenoid allows an exceptional induction of autophagy, in particular a significant reduction of the protein level of mutant huntingtin, a significant reduction of the protein level of A53T ?-synuclein, a significant inhibition of the oligomerization of ?-synuclein and a significant inhibition of the inclusion formation of huntingtin via the AMPK-mTOR dependent autophagy inducing pathway.

Abstract: A method for inhibiting the expression and/or functional activity of an ABC transporter protein in a subject suffering from a disorder associated with an overexpression of the ABC transporter protein includes administrating a cobalt-polypyridyl complex to the subject. A method for inhibiting the expression and/or functional activity of an ABC transporter in cells includes contacting the cells with an effective amount of the cobalt-polypyridyl complex.

Abstract: A method for treating a subject suffering from a cancer, in particular a multidrug-resistant cancer includes administrating a cobalt-polypyridyl complex to the subject. A method for suppressing the growth of cancer cells, in particular inducing autophagy of the cancer cells, inducing cell cycle arrest of the cancer cells and/or inhibiting cell invasion of the cancer cells and for specifically targeting cancer cells with multidrug-resistance includes contacting said cancer cells with the cobalt-polypyridyl complex. A pharmaceutical composition and a kit are provided and include the cobalt-polypyridyl complex. Unexpectedly, the cobalt-polypyridyl complex is especially suitable to treat cancer, in particular multidrug-resistant cancer with an exceptionally increased cytotoxic activity towards multidrug-resistant cancer cells.

Abstract: A method for treating a subject suffering from a cancer, in particular a multidrug-resistant cancer includes administrating a cobalt-polypyridyl complex to the subject. A method for suppressing the growth of cancer cells, in particular inducing autophagy of the cancer cells, inducing cell cycle arrest of the cancer cells and/or inhibiting cell invasion of the cancer cells and for specifically targeting cancer cells with multidrug-resistance includes contacting said cancer cells with the cobalt-polypyridyl complex. A pharmaceutical composition and a kit are provided and include the cobalt-polypyridyl complex. Unexpectedly, the cobalt-polypyridyl complex is especially suitable to treat cancer, in particular multidrug-resistant cancer with an exceptionally increased cytotoxic activity towards multidrug-resistant cancer cells.

Abstract: The present invention provides methods for treatment of a RAS-positive disease, in particular KRAS-positive non-small cell lung cancer as well as a method for potentiating the apoptotic activity of a PDE? inhibitor by combining the PDE? inhibitor with a direct autophagy inhibitor. The PDE? inhibitor is preferably, but not exclusively, deltarasin, and the direct autophagy inhibitor is in particular 3-methyladenine. Further provided by the present invention are a kit and a pharmaceutical composition comprising the PDE? inhibitor and a direct autophagy inhibitor. The methods of the present invention in particular provide a new treatment option for RAS-positive diseases such as KRAS-positive non-small cell lung cancer allowing for an increased apoptotic activity of the PDE? inhibitor by simultaneously blocking its “tumor protective” autophagy.

Abstract: One example embodiment relates to a method of treating lung cancer by administering a compound of formula I to a subject in need thereof. Another embodiment relates to a method to treat Non-Small Cell Lung Cancer (NSCLC) by administering the compound of formula I to a patient.

Abstract: The present invention discloses a method of treating cancer and/or multidrug-resistant cancer, comprising administering an effective amount of hernandezine or thalidezine. A pharmaceutical composition comprising hernandezine or thalidezine admixed with a pharmaceutical carrier for treating cancers and/or multidrug-resistant cancer is also disclosed.

Abstract: Prenylated isoflavones are suitable to specifically inhibit P-glycoprotein in multidrug-resistant cancer cells leading to an accumulation of cytotoxic compounds or therapeutic compounds in the cells while having exceptionally increased cytotoxic activity specifically towards multidrug-resistant cancer cells and while allowing for an increased activity of chemotherapeutic compounds towards which the cells are resistant. Also in accordance with the present invention is a method for specifically targeting cancer cells with multidrug-resistance as well as a method of potentiating the activity of a chemotherapeutic compound in multidrug-resistant cancer cells. In a further aspect, a kit including a prenylated isoflavone and a chemotherapeutic compound is provided.

Abstract: A quinonemethide triterpenoid is administered to subjects with multidrug-resistant cancer, in particular a cancer with enhanced expression and/or functional activity of ABC transporter proteins such as P-glycoprotein and/or an apoptosis-deficient, in particular p53-, Bax- or Bak-deficient, cancer, i.e. specific subgroups of subjects with cancer. The quinonemethide triterpenoid is suitable to treat cancer allowing for an accumulation of cytotoxic or therapeutic compounds in the cells while having exceptionally increased cytotoxic activity towards the multidrug-resistant cancer cells and while allowing for an increased activity of chemotherapeutic compounds. Methods for specifically targeting cancer cells with multidrug-resistance and methods for potentiating the activity of a chemotherapeutic compound in those cancer cells are also disclosed. A kit including a quinonemethide triterpenoid and a chemotherapeutic compound is also provided.

Abstract: The present invention discloses a method of treating cancer and/or multidrug-resistant cancer, comprising administering an effective amount of hernandezine or thalidezine. A pharmaceutical composition comprising hernandezine or thalidezine admixed with a pharmaceutical carrier for treating cancers and/or multidrug-resistant cancer is also disclosed.

Abstract: The present invention discloses a method of treating cancer comprising administering an effective amount of an alkaloid, in which the alkaloid is liensinine, isoliensinine, dauricine, cepharanthine, hernandezine or thalidezine and isolated from the traditional Chinese medicinal herbs. The use of the alkaloid in treating neurodegenerative disorder is also disclosed.

Abstract: The present invention discloses a method of treating cancer comprising administering an effective amount of an alkaloid, in which the alkaloid is liensinine, isoliensinine, dauricine, cepharanthine, hernandezine or thalidezine and isolated from the traditional Chinese medicinal herbs. The use of the alkaloid in treating neurodegenerative disorder is also disclosed.