Abstract: Systems and methods are provided for adaptive data replication. A first data object is stored. One or more first network characteristics of a communication network are detected. A first replication mode is triggered (e.g., a single-master replication mode) based on the one or more first network characteristics of the communication network. The single-master replication may be configured to facilitate real-time synchronizations (e.g., for critical updates). One or more second network characteristics of the communication network are detected. A second replication mode (e.g., a multi-master replication mode) is triggered based on the one or more second network characteristics. The second replication may be configured to facilitate a delayed synchronization (e.g., for non-critical updates) of the first data object and the second data object using the second update file.

Abstract: The invention relates to compounds of formula (I): or a salt thereof, wherein R1, G, L1, L2, L3, and Y are as described herein. Compounds of formula (I) and pharmaceutical compositions thereof are inhibitors of one, or both of, ?v?1 integrin and ?v?6 integrin that are useful for treating fibrosis such as in nonalcoholic steatohepatitis (NASH), idiopathic pulmonary fibrosis (IPF) and nonspecific interstitial pneumonia (NSIP).

Abstract: A user equipment (UE) is configured to transmit, to a cellular carrier, a request to activate the UE with the cellular carrier. The UE is also configured to, in response to receiving an authentication request for authenticating a user of the UE, transmit, to the cellular carrier, information identifying another UE and authentication information for authenticating the user ; prompt the user, via a display of the UE, to provide, to an input system of the UE, verification information transmitted to the other UE; transmit, to the cellular carrier, the verification information; and in response to validation of the verification information by the cellular carrier, receive an embedded subscriber identity module (eSIM) subscription transferred from the other UE.

Abstract: The present invention relates to the identification of fibrinogen like protein 1 (FGL1) as a prognostic biomarker for responsiveness to an immune checkpoint inhibitor in a cancer patient. More specifically it relates to methods of treating cancer in a human patient comprising administering an immune checkpoint inhibitory antibody specifically inhibiting the interaction of fibrinogen-like protein 1 (FGL1) with lymphocyte-activation gene 3 protein (LAG3), wherein the cancer is an FGL1 expressing cancer. Further, the invention relates to methods for assessing susceptibility or predicting the responsiveness to the treatment with an immune checkpoint inhibitory antibody specifically inhibiting the interaction of FGL1 with LAG3 in a cancer patient, comprising detecting FGL1 expression in a sample from said patient and to a kit for selecting a cancer patient that would benefit from an immune checkpoint inhibitory antibody specifically inhibiting the interaction of FGL1 with LAG3.

Abstract: Methods of treating neuronal disorders, such as mechanical neuronal traumas and neurodegenerative disorders, with TWEAK or a TWEAK receptor blocking agents are presented.

Abstract: The present invention provides methods and agents for the treatment of TWEAK-related conditions, including cardiac, liver, kidney, lung, adipose, skeletal, muscle, neuronal, bone and cartilage conditions. The invention also provides methods for identifying TWEAK agonists or antagonists for the treatment of TWEAK-related conditions. Additionally, the invention provides transgenic animals that express an exogenous DNA encoding a TWEAK polypeptide, or fragments, analogs, or muteins thereof, and methods for using such animals to identify TWEAK agonists or antagonists. The invention further provides methods for diagnosing a disease based on TWEAK expression. The invention also provides methods for affecting cellular differentiation of progenitor cells using TWEAK polypeptides, agonists, or antagonists.

Abstract: The present invention provides methods and agents for the treatment of TWEAK-related conditions, including cardiac, liver, kidney, lung, adipose, skeletal, muscle, neuronal, bone and cartilage conditions. The invention also provides methods for identifying TWEAK agonists or antagonists for the treatment of TWEAK-related conditions. Additionally, the invention provides transgenic animals that express an exogenous DNA encoding a TWEAK polypeptide, or fragments, analogs, or muteins thereof, and methods for using such animals to identify TWEAK agonists or antagonists. The invention further provides methods for diagnosing a disease based on TWEAK expression. The invention also provides methods for affecting cellular differentiation of progenitor cells using TWEAK polypeptides, agonists, or antagonists.

Abstract: Methods of treating inflammatory disorders, such as rheumatoid arthritis, by modulating TWEAK and TNF-? are disclosed, as are other methods.

Abstract: The present invention provides methods and agents for the treatment of TWEAK-related conditions, including cardiac, liver, kidney, lung, adipose, skeletal, muscle, neuronal, bone and cartilage conditions. The invention also provides methods for identifying TWEAK agonists or antagonists for the treatment of TWEAK-related conditions. Additionally, the invention provides transgenic animals that express an exogenous DNA encoding a TWEAK polypeptide, or fragments, analogs, or muteins thereof, and methods for using such animals to identify TWEAK agonists or antagonists. The invention further provides methods for diagnosing a disease based on TWEAK expression. The invention also provides methods for affecting cellular differentiation of progenitor cells using TWEAK polypeptides, agonists, or antagonists.

Abstract: The present invention provides methods and agents for the treatment of TWEAK-related conditions, including cardiac, liver, kidney, lung, adipose, skeletal, muscle, neuronal, bone and cartilage conditions. The invention also provides methods for identifying TWEAK agonists or antagonists for the treatment of TWEAK-related conditions. Additionally, the invention provides transgenic animals that express an exogenous DNA encoding a TWEAK polypeptide, or fragments, analogs, or muteins thereof, and methods for using such animals to identify TWEAK agonists or antagonists. The invention further provides methods for diagnosing a disease based on TWEAK expression. The invention also provides methods for affecting cellular differentiation of progenitor cells using TWEAK polypeptides, agonists, or antagonists.

Abstract: Methods of treating neuronal disorders, such as mechanical neuronal traumas and neurodegenerative disorders, with TWEAK or a TWEAK receptor blocking agents are presented.

Abstract: Methods of treating inflammatory disorders, such as rheumatoid arthritis, by modulating TWEAK and TNF-? are disclosed, as are other methods.

Abstract: The present invention provides methods and agents for the treatment of TWEAK-related conditions, including cardiac, liver, kidney, lung, adipose, skeletal, muscle, neuronal, bone and cartilage conditions. The invention also provides methods for identifying TWEAK agonists or antagonists for the treatment of TWEAK-related conditions. Additionally, the invention provides transgenic animals that express an exogenous DNA encoding a TWEAK polypeptide, or fragments, analogs, or muteins thereof, and methods for using such animals to identify TWEAK agonists or antagonists. The invention further provides methods for diagnosing a disease based on TWEAK expression. The invention also provides methods for affecting cellular differentiation of progenitor cells using TWEAK polypeptides, agonists, or antagonists.

Abstract: The present invention relates to methods of modulating angiogenesis and inhibiting tumor progression by using TWEAK receptor (Fn14) agonists. In particular, methods for inhibiting angiogenesis are disclosed.

Abstract: The present invention relates to methods of modulating angiogenesis and inhibiting tumor progression by using TWEAK receptor (Fn14) agonists. In particular, methods for inhibiting angiogenesis are disclosed.

Abstract: Methods of modulating TL1A for the treatment of disease are disclosed.

Abstract: The present invention provides methods and agents for the treatment of TWEAK-related conditions, including cardiac, liver, kidney, lung, adipose, skeletal, muscle, neuronal, bone and cartilage conditions. The invention also provides methods for identifying TWEAK agonists or antagonists for the treatment of TWEAK-related conditions. Additionally, the invention provides transgenic animals that express an exogenous DNA encoding a TWEAK polypeptide, or fragments, analogs, or muteins thereof, and methods for using such animals to identify TWEAK agonists or antagonists. The invention further provides methods for diagnosing a disease based on TWEAK expression. The invention also provides methods for affecting cellular differentiation of progenitor cells using TWEAK polypeptides, agonists, or antagonists.

Abstract: Methods of treating neuronal disorders, such as mechanical neuronal traumas and neurodegenerative disorders, with TWEAK or TWEAK-R blocking agents are presented.

Abstract: Methods of treating inflammatory disorders, such as rheumatoid arthritis, by modulating TWEAK and TNF-? are disclosed, as are other methods.

Abstract: The present invention relates to methods of modulating angiogenesis and inhibiting tumor progression by using TWEAK receptor (Fn14) agonists. In particular, methods for inhibiting angiogenesis are disclosed.