Abstract: The disclosure is directed to novel predictive methods and personalized therapies for treating dry eye disease (DED). Specifically, this disclosure relates to methods of treating a patient having DED by selectively administering a TNF? antagonist, e.g., a TNF? antibody, such as LME636, to the patient on the basis of that patient being genetically predisposed to have a favorable response to treatment with the TNF? antagonist. Also disclosed herein are transmittable forms of information, diagnostic methods, and kits useful in predicting the likelihood that a patient having DED will respond to treatment with a TNF? antagonist, e.g., a TNF? antibody, such as LME636.

Abstract: The invention provides methods for predicting therapeutic responsiveness of a subject suffering from cognitive impairments or dysfunctions, psychotic and/or neurodegenerative disorders to an alpha 7 nicotinic acetylcholine receptor activator treatment.

Abstract: The disclosure is directed to novel predictive methods and personalized therapies for treating dry eye disease (DED). Specifically, this disclosure relates to methods of treating a patient having DED by selectively administering a TNF? antagonist, e.g., a TNF? antibody, such as LME636, to the patient on the basis of that patient being genetically predisposed to have a favorable response to treatment with the TNF? antagonist. Also disclosed herein are transmittable forms of information, diagnostic methods, and kits useful in predicting the likelihood that a patient having DED will respond to treatment with a TNF? antagonist, e.g., a TNF? antibody, such as LME636.

Abstract: Disclosed herein are methods of treatment or prevention of acute anxiety in an individual in need thereof. Such methods include administering to the individual an alpha 7 nicotinic acetylcholine receptor (?7 nAChR) modulator at a therapeutic dose to treat or prevent manifestations of the acute anxiety and symptoms thereof.

Abstract: Disclosed herein is a method of treatment or prevention of public speaking anxiety (PSA), which may in some cases present as a symptom of social anxiety disorder (SAD), including the performance only (SAD-PO) subtype of SAD. The method of treatment includes administering an a7 nAChR agonist such as (R)-3-(6-p-tolyl-pyridin-3-yloxy)-1-aza-bicyclo[2.2.2]octane to the individual at a therapeutically effective dose.

Abstract: The invention features methods of identifying patients as being likely to respond to anti-VEGF therapy. Furthermore, in those patients identified as failing to include one or more of the above ophthalmic response markers, the invention features treatment with an EPO antagonist (e.g., alone, or in combination with a VEGF antagonist).

Abstract: The invention provides methods for predicting therapeutic responsiveness of a subject suffering from cognitive impairments or dysfunctions, psychotic and/or neurodegenerative disorders to an alpha 7 nicotinic acetylcholine receptor activator treatment.

Abstract: The invention provides methods for predicting therapeutic responsiveness of a subject suffering from cognitive impairments or dysfunctions, psychotic and/or neurodegenerative disorders to an alpha 7 nicotinic acetylcholine receptor activator treatment.

Abstract: The invention features methods of identifying patients as being likely to respond to anti-VEGF therapy. Furthermore, in those patients identified as failing to include one or more of the above ophthalmic response markers, the invention features treatment with an EPO antagonist (e.g., alone, or in combination with a VEGF antagonist).

Abstract: The disclosure is directed to novel predictive methods and personalized therapies for treating dry eye disease (DED). Specifically, this disclosure relates to methods of treating a patient having DED by selectively administering a TNF? antagonist, e.g., a TNF? antibody, such as LME636, to the patient on the basis of that patient being genetically predisposed to have a favorable response to treatment with the TNF? antagonist. Also disclosed herein are transmittable forms of information, diagnostic methods, and kits useful in predicting the likelihood that a patient having DED will respond to treatment with a TNF? antagonist, e.g., a TNF? antibody, such as LME636.

Abstract: The invention features methods of identifying patients as being likely to respond to anti-VEGF therapy. Furthermore, in those patients identified as failing to include one or more of the above ophthalmic response markers, the invention features treatment with an EPO antagonist (e.g., alone, or in combination with a VEGF antagonist).

Abstract: The invention provides methods for predicting therapeutic responsiveness of a subject suffering from cognitive impairments or dysfunctions, psychotic and/or neurodegenerative disorders to an alpha 7 nicotinic acetylcholine receptor activator treatment.

Abstract: The invention provides methods for predicting therapeutic responsiveness of a subject suffering from cognitive impairments or dysfunctions, psychotic and/or neurodegenerative disorders to an alpha 7 nicotinic acetylcholine receptor activator treatment.

Abstract: Pharmacogenetic analysis revealed an effect of risk alleles in ARMS2 and CFH genes on the response of subjects to anti-C5 antibodies in the treatment of the progression of geographic atrophy.

Abstract: The invention provides methods for predicting therapeutic responsiveness of a subject suffering from cognitive impairments or dysfunctions, psychotic and/or neurodegenerative disorders to an alpha 7 nicotinic acetylcholine receptor activator treatment.

Abstract: Embodiments are directed to establishing a fault tolerant parallel database system and to detecting the health of parallel database services. In an embodiment, a computer system establishes a control node cluster that includes at least one active control node and at least one spare control node. Each node of the control node cluster includes specific functions assumable only by other control nodes. The computer system also establishes a compute node cluster that includes at least one active computing node, at least one spare computing node, at least one active storage node and at least one spare storage node. Each of the computing and storage nodes includes specific functions assumable only by other computing and storage nodes. The computer system detects a failure of an active node and instantiates a corresponding spare node that is configured to perform the functions of the failed active node.

Abstract: The invention is directed to the use of biomarkers to determine responsiveness of an individual with Fragile X Syndrome (FXS) to treatment with an mGluR5 antagonist.

Abstract: Embodiments are directed to establishing a fault tolerant parallel database system and to detecting the health of parallel database services. In an embodiment, a computer system establishes a control node cluster that includes at least one active control node and at least one spare control node. Each node of the control node cluster includes specific functions assumable only by other control nodes. The computer system also establishes a compute node cluster that includes at least one active computing node, at least one spare computing node, at least one active storage node and at least one spare storage node. Each of the computing and storage nodes includes specific functions assumable only by other computing and storage nodes. The computer system detects a failure of an active node and instantiates a corresponding spare node that is configured to perform the functions of the failed active node.

Abstract: The genetic polymorphism LRRK2 (leucine-rich repeat kinase 2)-T1602S is significantly associated with conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD), with the patients with TT genotype being at greater risk to progress to Alzheimer's disease. The LRRK2-T2352 also showed a trend for conversion to Alzheimer's disease, with the patients with CC genotype tending to progress to Alzheimer's disease. Similar to the APOE-E4 allele, in the presence of a BuChE-K variant, LRRK2-T1602S and LRRK2-T2352 showed a greater association with the rate of conversion from mild cognitive impairment to Alzheimer's disease. In another study with placebo-treated Alzheimer's disease patients, LRRK2-T1602S and LRRK2-T2352 showed a same trend of association. The Alzheimer's disease patients with TT genotype of LRRK2-T1602S or CC genotype of LRRK2-T2352 tended to decline faster on cognitive performance over 6 months, especially in the presence of a BuChE-K variant.

Abstract: This invention provides methods to predict the likelihood of suicidal or self-destructive behaviour in a patient during treatment. The method employs the detection of a VNTR polymorphism in the 3?-UTR of the dopamine transporter gene (SLC6A3). Patients with nine or fewer repeats are considered poor responders to clozapine. Nine or fewer repeats in the SLC6A3 gene have been correlated with poor expression of the SLC6A3 gene. Also provided are methods of treatment based on the presence or absence of this polymorphism or surrogate markers thereof. Also provided are kits to use in the methods of the invention.