Abstract: Described herein are devices, systems and method of treating inflammation by vagus nerve stimulation and the delivery of an anti-inflammatory drug. In particular, described herein are methods of treating inflammation including the steps of stimulating a subject's inflammatory reflex to inhibit the immune response and administering an anti-inflammatory drug.

Abstract: There is disclosed a pharmaceutical composition and method for treating sepsis, including septic shock and ARDS (acute respiratory distress syndrome), comprising administering an effective amount of a HMG1 antagonist. There is further disclosed a diagnostic method for monitoring the severity or potential lethality of sepsis or septic shock, comprising measuring the serum concentration of HMG1 in a patient exhibiting or at risk of exhibiting sepsis or septic shock symptoms. Lastly, there is disclosed a pharmaceutical composition and method for effecting weight loss or treating obesity, comprising administering an effective amount of HMG1 or a therapeutically active HMG1 fragment.

Abstract: Methods of inhibiting release of a proinflammatory cytokine from a macrophage are provided. The methods comprise treating the macrophage with a cholinergic agonist in an amount sufficient to decrease the amount of the proinflammatory cytokine that is released from the macrophage, wherein the cholinergic agonist is selective for an ?7 nicotinic receptor. Methods for inhibiting an inflammatory cytokine cascade in a patient are also provided. The methods comprise treating the patient with a cholinergic agonist in an amount sufficient to inhibit the inflammatory cytokine cascade, wherein the cholinergic agonist is selective for an ?7 nicotinic receptor. Methods for determining whether a compound is a cholinergic agonist reactive with an ?7 nicotinic receptor are also provided. The methods comprise determining whether the compound inhibits release of a proinflammatory cytokine from a mammalian cell.

Abstract: Isolated SAA peptides, fusion proteins and compositions comprising such are provided as are domain-specific SAA antibodies. Methods of treating sepsis and endotoxemia are also provided.

Abstract: Isolated SAA peptides, fusion proteins and compositions comprising such are provided as are domain-specific SAA antibodies. Methods of treating sepsis and endotoxemia are also provided.

Abstract: Described herein are devices, systems and method for treating inflammatory disorders by modulating a subject's inflammatory reflex. The method may include the step of non-invasively stimulating the inflammatory reflex (e.g., the vagus nerve, the splenic nerve, the hepatic nerve, the facial nerve, and the trigeminal nerve) of a subject in a manner which significantly reduces proinflammatory cytokines in the subject and/or provides a therapeutically effective treatment for the subject. Devices for non-invasively stimulating the inflammatory reflex may include a movable tip or actuator that is controlled to mechanically stimulate the ear. The devices may be hand-held or wearable, and may stimulate the cymba conchae region of the subject's ear.

Abstract: Described herein are devices, systems and method of treating inflammation by vagus nerve stimulation and the delivery of an anti-inflammatory drug. In particular, described herein are methods of treating inflammation including the steps of stimulating a subject's inflammatory reflex to inhibit the immune response and administering an anti-inflammatory drug.

Abstract: Methods of inhibiting release of a proinflammatory cytokine from a macrophage are provided. The methods comprise treating the macrophage with a cholinergic agonist in an amount sufficient to decrease the amount of the proinflammatory cytokine that is released from the macrophage, wherein the cholinergic agonist is selective for an ?7 nicotinic receptor. Methods for inhibiting an inflammatory cytokine cascade in a patient are also provided. The methods comprise treating the patient with a cholinergic agonist in an amount sufficient to inhibit the inflammatory cytokine cascade, wherein the cholinergic agonist is selective for an ?7 nicotinic receptor. Methods for determining whether a compound is a cholinergic agonist reactive with an ?7 nicotinic receptor are also provided. The methods comprise determining whether the compound inhibits release of a proinflammatory cytokine from a mammalian cell.

Abstract: Described herein are devices, systems and method of treating inflammation, including methods of treating a T-cell mediated disease. In particular, described herein are methods of treating inflammation including the steps of stimulating a subject's inflammatory reflex to inhibit the immune response and administering a T-cell modifying agent to modify the activity of splenic T-cells. Also described herein are systems for treating inflammation including an inflammatory reflex stimulation module and a T-cell response modifying module. The T-cell response modifying module typically modifies the response of splenic T-cells to enhance or otherwise regulate the effect of stimulation of the inflammatory reflex.

Abstract: Disclosed are therapeutic beads comprising agents, such as nucleic acids, that bind to high mobility group box 1 (HMGB1) and methods of treating subjects with conditions that would benefit from reducing the deleterious effects of HMGB1, such as inflammatory bowel diseases, comprising administering the beads to the gastrointestinal tract of the subjects.

Abstract: A method of inhibiting the release of a proinflammatory cytokine in a cell is disclosed. The method comprises treating the cell with a cholinergic agonist. The method is useful in patients at risk for, or suffering from, a condition mediated by an inflammatory cytokine cascade, for example endotoxic shock. The cholinergic agonist treatment can be effected by stimulation of an efferent vagus nerve fiber, or the entire vagus nerve.

Abstract: Isolated SAA peptides, fusion proteins and compositions comprising such are provided as are domain-specific SAA antibodies. Methods of treating sepsis and endotoxemia are also provided.

Abstract: A method of inhibiting the release of a proinflammatory cytokine in a cell is disclosed. The method comprises treating the cell with a cholinergic agonist. The method is useful in patients at risk for, or suffering from, a condition mediated by an inflammatory cytokine cascade, for example endotoxic shock. The cholinergic agonist treatment can be effected by stimulation of an efferent vagus nerve fiber, or the entire vagus nerve.

Abstract: A method of treating a fatty liver disease in a subject. The method comprises administering to the subject an effective amount of a cholinergic pathway stimulating agent, wherein the fatty liver disease is selected from non-alcoholic fatty liver (NAFL), alcoholic fatty liver (AFL), non-alcoholic steatohepatitis (NASH), alcoholic steatohepatitis (ASH), NASH-associated liver fibrosis, ASH-associated liver fibrosis, non-alcoholic cirrhosis, and alcoholic cirrhosis.

Abstract: There is disclosed a pharmaceutical composition and method for treating sepsis, including septic shock and ARDS (acute respiratory distress syndrome), comprising administering an effective amount of a HMG1 antagonist. There is further disclosed a diagnostic method for monitoring the severity or potential lethality of sepsis or septic shock, comprising measuring the serum concentration of HMG1 in a patient exhibiting or at risk of exhibiting sepsis or septic shock symptoms. Lastly, there is disclosed a pharmaceutical composition and method for effecting weight loss or treating obesity, comprising administering an effective amount of HMG1 or a therapeutically active HMG1 fragment.

Abstract: Compounds of Formula (I), pharmaceutical compositions comprising compounds of Formulae (I a) or (VII) and a method of treating a subject with an inflammatory cytokine-mediated disorder comprising administering to the subject a compound of Formulae (I a) or (VIIa). The variables of Formulae (I), (I a), (VII) and (VII a) are described herein.

Abstract: Disclosed is a method of reducing bleed time in a subject by activation of the cholinergic anti-inflammatory pathway in said subject. The cholinergic anti-inflammatory pathway can be activated by direct or indirect stimulation of the vagus nerve. The cholinergic anti-inflammatory pathway can also be activated by administering an effective amount of cholinergic agonist or acetylcholinesterase inhibitor to the subject.

Abstract: An antibody or an antigen binding fragment thereof which binds to mammalian ?7 subunit of a nicotinic acetylcholine receptor or its functional variant and which is an agonist of said receptor or variant. Pharmaceutical compositions comprising same. A method of treating a subject suffering from an inflammatory condition comprising administering to said subject an antibody or an antigen-binding fragment as described herein.

Abstract: Compositions and methods are disclosed for inhibiting the release of a proinflammatory cytokine from a vertebrate cell, and for inhibiting an inflammatory cytokine cascade in a patient. The compositions comprise a vertebrate HMGB A box, and an antibody preparation that specifically binds to a vertebrate HMGB B box. The methods comprise treating a cell or a patient with sufficient amounts of the composition to inhibit the release of the proinflammatory cytokine, or to inhibit the inflammatory cytokine cascade.

Abstract: Described herein are methods, devices and systems for inhibition of granulocyte activation by appropriate stimulation of the vagus nerve. Methods of treating granulocyte-mediated disorders (including inflammatory disorders) by stimulating the vagus nerve to inhibit granulocyte activation (particularly neutrophil activation) are also described. Appropriate stimulation may be very low levels of stimulation, including stimulation that does not result in desensitization. The level of granulocyte activation may be detected and used to at least partially control stimulation.