Abstract: The present disclosure relates to the treatment of agitation caused by noradrenergic hyperarousal in an agitated subject. The present disclosure provides oromucosal dosage forms comprising effective amounts of latrepirdine either alone or in combination with dexmedetomidine or pharmaceutically acceptable salts thereof and one or more pharmaceutically acceptable carriers and/excipients. Methods of their use are also provided. The present disclosure also provides a method of treating depression by administering oromucosally a therapeutically effective amount of dexmedetomidine alone or in combination with latrepirdine.

Abstract: Disclosed herein are methods and composition for treating bipolar disorders and psychosis by administering dexmedetomidine. The methods and composition alleviate mania, hypomania, psychosis, and depression in the subjects, providing improved therapeutic outcomes.

Abstract: Disclosed in the present disclosure is a method, system and apparatus for prediction, estimation and prevention of occurrence of agitation episode in a subject predisposed to agitation. The method comprises receiving, from a first monitoring device attached to a subject, physiological data of sympathetic nervous system activity in the subject and activity data of the subject; receiving, from a computing device, a plurality of indications associated with a plurality of agitation episodes of the subject; analyzing, using at least one machine learning model, the physiological data, the activity data, and the plurality of indications to determine a probability of an occurrence of an agitation episode of the subject; and sending a signal to a second monitoring device to notify the second monitoring device of the probability of the occurrence of the agitation episode of the subject such that treatment can be provided to the subject to decrease sympathetic nervous system activity in the subject.

Abstract: In some embodiments, a method includes receiving first physiological data of sympathetic nervous system activity and establishing a baseline value of at least one physiological parameter by training at least one machine learning model using the first physiological data. The method further includes receiving, from a first monitoring device attached to a subject, second physiological data of sympathetic nervous system activity in the subject. Using the at least one machine learning model and based on the baseline value of at least one physiological parameter, the method includes analyzing the second physiological data to predict an agitation episode of the subject and sending a signal to a second monitoring device to notify of the prediction of the agitation episode of the subject such that treatment can be provided to the subject to decrease sympathetic nervous system activity in the subject.

Abstract: The method for determining mutual voltage sensitivity coefficients between a plurality of measuring nodes of an electric power network does not rely on knowledge of the network parameters (for example: series conductance and susceptance of the branches, shunt conductance and susceptance of the nodes, etc.). The method uses a monitoring infrastructure including metering units at each one of the measuring nodes, and includes a step of measuring at the same time, at each one of the measuring nodes, repeatedly over a time window, sets of data including values of the current, the voltage, and the phase difference, a step of computing active power, reactive power and values from each set of measured data, and a step of performing multiple parametric regression analysis of the variations of the voltage at each one of the measuring nodes.

Abstract: The method for determining mutual voltage sensitivity coefficients between a plurality of measuring nodes of an electric power network does not rely on knowledge of the network parameters (for example: series conductance and susceptance of the branches, shunt conductance and susceptance of the nodes, etc.). The method uses a monitoring infrastructure including metering units at each one of the measuring nodes, and includes a step of measuring at the same time, at each one of the measuring nodes, repeatedly over a time window, sets of data including values of the current, the voltage, and the phase difference, a step of computing active power, reactive power and values from each set of measured data, and a step of performing multiple parametric regression analysis of the variations of the voltage at each one of the measuring nodes.

Abstract: PDE4 inhibition is achieved by novel compounds, e.g., N-substituted aniline and diphenylamine analogs. The compounds of the present invention are of Formula I: wherein R1, R2, R3and R4 are as defined herein.

Abstract: The present invention relates to methods of treatment using the compound (+)-isopropyl 2-methoxyethyl 4-(2-chloro-3-cyano-phenyl)-1,4-dihydro-2,6-dimethyl-pyridine-3,5-dicarboxylate, as a sole active agent or in combination with other pharmacological agents.

Abstract: The present invention relates e.g., to QM-7 or QT-6 cells comprising a heterologous mutant nicotinic ?7 acetylcholine receptor and/or a nucleic acid encoding it, or a fragment or variant thereof. In a preferred embodiment, the mutant nicotinic ?7 acetylcholine receptor subunit has a mutation in the M2 domain. QM-7 and QT-6 cells of the invention are useful for, e.g., assays such as high throughput assays that measure the influx of cations, such as Ca++ ions, into a cell. Such assays can be used, e.g., to identify agents that modulate the expression and/or activity of a mutant cell-surface-expressed channel receptor (e.g., the nicotinic ?7 receptor), and which thus modulate, e.g., among other functions, processes involved in the central nervous system, such as learning and memory.

Abstract: The present invention relates to methods of treatment using the compound (+)-isopropyl 2-methoxyethyl 4-(2-chloro-3-cyano-phenyl)-1,4-dihydro-2,6-dimethyl-pyridine-3,5-dicarboxylate, as a sole active agent or in combination with other pharmacological agents.

Abstract: PDE4 inhibition is achieved by novel compounds, e.g., N-substituted aniline and diphenylamine analogs. The compounds of the present invention are of Formula I: wherein R1, R2, R3 and R4 are as defined herein.

Abstract: PDE4 inhibition is achieved by novel compounds, e.g., N-substituted aniline and diphenylamine analogs. The compounds of the present invention are of Formula I: wherein R1, R2, R3and R4 are as defined herein.

Abstract: The present invention provides for a recombinant nucleic acid molecule comprising a humanized mouse ?-amyloid precursor protein (“APP”) gene comprising K670N, M671L and V717F mutations and uses thereof. The present invention further provides for a recombinant nucleic acid molecule comprising a region of a calcium-calmodulin dependent kinase II? (“CaMKII?”) promoter operatively linked to a ?-amyloid precursor protein (“APP”) gene comprising at least one mutation and uses thereof.

Abstract: Abstract of the Disclosure Human, rat and mouse cAMP phosphodiesterase isoforms (denoted PDE4D7s), as well as the DNA (RNA) encoding such polypeptides, are disclosed. Also disclosed are methods for utilizing such polypeptides in diagnostic assays for identifying mutations in nucleic acid sequences encoding the polypeptides of the present invention, for detecting altered levels of the polypeptide of the present invention as a means of detecting diseases and methods of screening potential modulators, especially inhibitors, of the novel PDE4D7s disclosed herein. Such as inhibitors can be used, for example, as a means of increasing cyclic AMP in neurons and thus treating neurological problems, such as long term memory loss, if not preventing such maladies entirely. Transgenic animals expressing polypeptides disclosed herein are also described.

Abstract: PDE4 inhibition is achieved by novel compounds, e.g., N-substituted aniline and diphenylamine analogs.

Abstract: PDE4 inhibition is achieved by novel compounds, e.g., N-substituted aniline and diphenylamine analogs. The compounds of the present invention are of Formula I: wherein R1, R2 , R3 and R4 are as defined herein.

Abstract: The present invention relates e.g., to QM-7 or QT-6 cells comprising a heterologous mutant nicotinic &agr;7 acetylcholine receptor and/or a nucleic acid encoding it, or a fragment or variant thereof. In a preferred embodiment, the mutant nicotinic &agr;7 acetylcholine receptor subunit has a mutation in the M2 domain. QM-7 and QT-6 cells of the invention are useful for, e.g., assays such as high throughput assays that measure the influx of cations, such as Ca++ ions, into a cell. Such assays can be used, e.g., to identify agents that modulate the expression and/or activity of a mutant cell-surface-expressed channel receptor (e.g., the nicotinic &agr;7 receptor), and which thus modulate, e.g., among other functions, processes involved in the central nervous system, such as learning and memory.

Abstract: PDE4 inhibition is achieved by novel compounds, e.g., N-substituted aniline and diphenylamine analogs.

Abstract: PDE4 inhibition is achieved by novel compounds, e.g., N-substituted aniline and diphenylamine analogs.

Abstract: Described herein are compounds having the general formula: ##STR1## wherein: Ar.sup.1 and Ar.sup.2 are independently selected aryl groups, optionally substituted with substituents selected from the group consisting of alkyl, cycloalkyl, alkoxy, alkanoyl, aralkyl, aralkyloxy, halo, NO.sub.2, Ph, CF.sub.3, CN, OH, methylenedioxy, ethylenedioxy, SO.sub.2 NRR', NRR', CO.sub.2 R (where R and R' are independently selected from the group consisting of H and alkyl) and a second aryl group, which may be substituted as above;wherein any cycloalkyl or aryl substituent is linked to Ar.sup.1 or Ar.sup.2 by a bridging element which may be a single bond, a vinylene group, an ethynylene group, a Z group, a --Z--(CH.sub.2).sub.n -- group, a --(CH.sub.2).sub.n --Z-- group, or a --Z--(CH.sub.2).sub.n --Z-- group, where Z represents an O atom, a S atom, an NH group or an N-alkyl group, and n is an integer from 1 to 4;wherein Ar.sup.1 and Ar.sup.