Abstract: In one example, the present disclosure describes various methods, computer-readable media, and apparatuses for supporting social engineering attack prevention based on early detection and remediation of various types of social engineering attacks which may be initiated within various contexts. In one example, supporting social engineering attack prevention may include identifying a workflow to be protected, identifying, for the workflow, a set of valid resources of the workflow where the set of valid resources includes a set of artifacts and a set of templates, identifying, from a dataset associated with the workflow and based on the set of artifacts, a communication associated with the workflow, determining, based on an analysis of the communication based on the set of templates, that the communication is malicious, and initiating, based on the determination that the communication is malicious, a remediation action.

Abstract: A graphene-based ion sensitive field effect transistor (GISFET) with high sensitivity and selectivity for ions is provided. For example, the GISFET of the present invention can exhibit high sensitivity and selectivity for K+ ions has been demonstrated utilizing a valinomycin-based ion selective membrane. The sensitivity of the GISFET can be at least about 50 millivolts/decade and can be stable for a time period of about two months, indicating the GISFET's reliability and effectiveness for physiological monitoring.

Abstract: Contextual awareness is used to reveal non-verbal expressions. A current context of a device is evaluated to infer a user's body posture and emotional state. The user's body posture and emotional state may then be used for improved services and targeted advertising.

Abstract: A graphene-based ion sensitive field effect transistor (GISFET) with high sensitivity and selectivity for ions is provided. For example, the GISFET of the present invention can exhibit high sensitivity and selectivity for K+ ions has been demonstrated utilizing a valinomycin-based ion selective membrane. The sensitivity of the GISFET can be at least about 50 millivolts/decade and can be stable for a time period of about two months, indicating the GISFET's reliability and effectiveness for physiological monitoring.

Abstract: The invention relates to treatment to restore normal metabolic function, including but not limited to normal glucose levels. The invention in one embodiment contemplates methods of reducing elevated glucose levels in subjects with elevated glucose levels by administering a composition comprising at least a portion of human Sfrp5. The invention in one embodiment contemplates methods of reducing elevated glucose levels in subjects with elevated glucose levels by administering a composition comprising an inhibitor of Wnt5a, including but not limited to an antibody inhibitor.

Abstract: As demonstrated herein, a preferential and progressive expansion of a subset of hematopoietic cells bearing somatic mutations in one or more HSC cardiometabolic driver genes leads to pro-inflammatory signaling at multiple levels. Accordingly, provided herein are compositions, methods, and assays for modulating a HSC cardiometabolic driver gene mutation-mediated proinflammatory activity.

Abstract: As demonstrated herein, a preferential and progressive expansion of a subset of hematopoietic cells bearing somatic mutations in TET2 leads to pro-inflammatory IL-1? signaling at multiple levels, including increased IL-1? transcription, increased NLRP3 inflammasome-mediated IL-1? secretion, and increased IL-1-Receptor 1-mediated IL-1? signaling. Accordingly, provided herein are compositions, methods, and assays for modulating TET2 mutation-mediated IL-1? (interleukin-1?) proinflammatory activity, particularly when caused by somatic mutations in TET2.

Abstract: As demonstrated herein, a preferential and progressive expansion of a subset of hematopoietic cells bearing somatic mutations in TET2 leads to pro-inflammatory IL-1? signaling at multiple levels, including increased IL-1? transcription, increased NLRP3 inflammasome-mediated IL-1? secretion, and increased IL-1-Receptor 1-mediated IL-1? signaling. Accordingly, provided herein are compositions, methods, and assays for modulating TET2 mutation-mediated IL-1? (interleukin-1?) proinflammatory activity, particularly when caused by somatic mutations in TET2.

Abstract: The invention relates to treatment to restore normal metabolic function, including but not limited to normal glucose levels. The invention in one embodiment contemplates methods of reducing elevated glucose levels in subjects with elevated glucose levels by administering a composition comprising at least a portion of human Sfrp5. The invention in one embodiment contemplates methods of reducing elevated glucose levels in subjects with elevated glucose levels by administering a composition comprising an inhibitor of Wnt5a, including but not limited to an antibody inhibitor.

Abstract: Contextual awareness is used to reveal non-verbal expressions. A current context of a device is evaluated to infer a user's body posture and emotional state. The user's body posture and emotional state may then be used for improved services and targeted advertising.

Abstract: Described herein are methods and compositions related to the discovery that the Follistatin-like 1 protein (Fstl-1) has metabolic and cardioprotective effects in vivo. Fstl-1 and portions and derivatives or variants thereof can be used to treat or prevent metabolic diseases or disorders and to treat or prevent cardiac damage caused by interrupted cardiac muscle blood supply.

Abstract: The present invention is directed to compositions and methods to treat an autoimmune disease in a subject, comprising an insulin-like 6 (Insl6) agent, such as an Insl6 polypeptide or variant or fragment thereof, or a nucleic acid encoding Insl6 poly peptide or variant or fragment thereof. Aspects of the present invention relate to use of Insl6 agents to reduce T-regulatory (Treg) cells in the subject and to reduce pro-inflammatory cytokines in a subject with an autoimmune disease such as a muscle autoimmune disease. The present invention also relates to methods and kits for the treatment of autoimmune diseases in a subject, and methods to diagnose a subject with an autoimmune disease such as myositis.

Abstract: Described herein are methods and compositions related to the discovery that the Follistatin-like 1 protein (Fstl-1) has metabolic and cardioprotective effects in vivo. Fstl-1 and portions and derivatives or variants thereof can be used to treat or prevent metabolic diseases or disorders and to treat or prevent cardiac damage caused by interrupted cardiac muscle blood supply.

Abstract: Described herein are methods and compositions related to the discovery that the Follistatin-like 1 protein (Fstl-1) has metabolic and cardioprotective effects in vivo. Fstl-1 and portions and derivatives or variants thereof can be used to treat or prevent metabolic diseases or disorders and to treat or prevent cardiac damage caused by interrupted cardiac muscle blood supply.

Abstract: The invention relates to treatment to restore normal metabolic function, including but not limited to normal glucose levels. The invention in one embodiment contemplates methods of reducing elevated glucose levels in subjects with elevated glucose levels by administering a composition comprising at least a portion of human Sfrp5. The invention in one embodiment contemplates methods of reducing elevated glucose levels in subjects with elevated glucose levels by administering a composition comprising an inhibitor of Wnt5a, including but not limited to an antibody inhibitor.

Abstract: The present invention relates to methods to identify factors associated with muscle growth, angiogenesis, obesity, insulin sensitivity body weight, fat mass, muscle mass and cardiovascular function. In particular, the methods of the present invention relates to assays to identify such factors using a transgenic animal model and/or a cell-based assay.

Abstract: Described herein are methods and compositions related to the discovery that the Follistatin-like 1 protein (Fstl-1) has metabolic and cardioprotective effects in vivo. Fstl-1 and portions and derivatives or variants thereof can be used to treat or prevent metabolic diseases or disorders and to treat or prevent cardiac damage caused by interrupted cardiac muscle blood supply.

Abstract: The present invention generally relates to methods, systems and computer readable media for the diagnosis and/or prognosis of a cardiac stress and/or skeletal muscle stress in a subject. In particular, in one embodiment, the methods, systems and computer readable media detect a level of Fstl expression, such as Fstl1 polypeptide or mRNA expression in a biological sample obtained from a subject, where a high level relative to a reference Fstl expression level is indicative of a subject having, or is at risk of cardiac stress and/or skeletal muscle stress. In such embodiments, the method futher comprises administering or undertaking an appropriate therapy in a subject identified to have or be at risk of cardiac stress and/or skeletal muscle stress.

Abstract: The present invention relates to metabolic regulators that affect metabolic function, for example metabolic regulators that affect muscle mass, muscle regeneration, muscle hypertrophy, fat mass, insulin and glucose sensitivity, angiogenesis and cardiovascular function. In particular, the present invention relates to modulating metabolic function by administering an effective amount of a pharmaceutical composition comprising an agent, where the agent activates or inhibits the activity and/or gene expression of the metabolic regulator. The metabolic regulators of the present invention are, for example MSP1 (2160028F08Rik; SEQ ID NO: 16); MSP2 (2310043I08Rik; SEQ ID NO: 17); MSP3 (NM_026754;1 110017116Rik; SEQ ID NO: 1); MSP4 (4732466D17Rik; SEQ BD NO: 18); MSP 5 (NM_024237; 1600015H20Rik; SEQ ID NO: 12); Ins16 (AF_156094; SEQ ID NO: 20). The present invention also provides methods to screen for agents that affect the metabolic regulators of the present invention.

Abstract: This invention relates to methods and compositions for the treatment of apoptotic cell-death. In particular the invention relates to Akt molecules and their use in inhibiting apoptotic cell-death in cardiomyocytes, skeletal myocytes and/or vascular endothelial cells. In view of these discoveries, Akt molecules can be used to inhibit apoptotic cell-death of any of the foregoing cells, and in particular, to treat conditions (e.g., myocardial infarction) that result in increased apoptotic cell-death of cardiomyocytes, skeletal myocytes and/or vascular endothelial cells.