Abstract: An electronic device caddy includes a first tray portion with at least two spaced lengthwise channels and an end cage and a second tray portion also including an end cage and at least two lengthwise rails slideable in the spaced channels of the first tray portion to load and accommodate different size electronic devices between the end cages. A locking mechanism releaseably locks at least one rail in its channel. A mounting bracket is attached rearward of one tray portion.

Abstract: Provided are methods of promoting browning of white adipose tissue (WAT) in a subject. Such methods can include administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of fexaramine in combination with a therapeutically effective amount of a compound that mimics or increases sympathetic nervous system activity (e.g., one or more beta-adrenergic agonists and/or compounds that increase epinephrine secretion).

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: This application provides methods of increasing vascularization, muscle performance, muscle rehabilitation, and/or mitochondrial activity in subjects in need thereof, by administering a therapeutically effective amount of one or more agents that increases ERR? activity to the subject. Such agents can include one or more ERR? agonists. In some examples the method does not require that the subject exercise, and as such, the subject may be sedentary (such as bedridden or in a wheelchair).

Abstract: The present disclosure provides FGF1 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Such mutant FGF1 proteins can be part of a chimeric protein that includes a ?-Klotho-binding protein, an FGFR1c-binding protein, a ?-Klotho-binding protein and a FGFR1c-binding protein, a C-terminal region from FGF19 or FGF21. In some examples, mutant FGF1 proteins have reduced mitogenic activity. Also provided are nucleic acid molecules that encode such proteins, and vectors and cells that include such nucleic acids. Methods of using the disclosed molecules to reduce blood glucose levels are also provided.

Abstract: The present invention relates to a chimeric protein that includes an N-terminus coupled to a C-terminus, where the N-terminus includes a portion of a paracrine fibroblast growth factor (“FGF”) and the C-terminus includes a C-terminal portion of an FGF19 molecule. The portion of the paracrine FGF is modified to decrease binding affinity for heparin and/or heparan sulfate compared to the portion without the modification. The present invention also relates to pharmaceutical compositions including chimeric proteins according to the present invention, methods for treating a subject suffering from diabetes, obesity, or metabolic syndrome, and methods of screening for compounds with enhanced binding affinity for the ?Klotho-FGF receptor complex involving the use of chimeric proteins of the present invention.

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: This application provides methods of increasing vascularization, muscle performance, muscle rehabilitation, and/or mitochondrial activity in subjects in need thereof, by administering a therapeutically effective amount of one or more agents that increases ERR? activity to the subject. Such agents can include one or more ERR? agonists. In some examples the method does not require that the subject exercise, and as such, the subject may be sedentary (such as bedridden or in a wheelchair).

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: The present invention relates to a chimeric protein that includes an N-terminus coupled to a C-terminus, where the N-terminus includes a portion of a paracrine fibroblast growth factor (“FGF”) and the C-terminus includes a C-terminal portion of an FGF19 molecule. The portion of the paracrine FGF is modified to decrease binding affinity for heparin and/or heparan sulfate compared to the portion without the modification. The present invention also relates to pharmaceutical compositions including chimeric proteins according to the present invention, methods for treating a subject suffering from diabetes, obesity, or metabolic syndrome, and methods of screening for compounds with enhanced binding affinity for the ?Klotho-FGF receptor complex involving the use of chimeric proteins of the present invention.

Abstract: Disclosed herein are methods for enhancing one or more effects of exercise in a subject by administering a PPAR? agonist (e.g., GW1516) to the subject in combination with an exercise program. Also disclosed are gene expression profiles unique to the combination of agonist-induced PPAR? activation and exercise. Such profiles are useful, at least, in methods for identifying the use of performance-enhancing drugs in exercised subjects (such as, professional or athletes). Direct interactions between PPAR? and exercised-induced kinases (e.g., AMPK or its subunits, AMPK ?1 and/or AMPK ?2) also are disclosed. Such protein-protein interactions provide new targets for identification of useful compounds.

Abstract: The method provides methods and compositions for treating metabolic disorders such as impaired glucose tolerance, elevated blood glucose, insulin resistance, dyslipidaemia, obesity, and fatty liver.

Abstract: This application provides methods of increasing vascularization, muscle performance, muscle rehabilitation, and/or mitochondrial activity in subjects in need thereof, by administering a therapeutically effective amount of one or more agents that increases ERR? activity to the subject. Such agents can include one or more ERR? agonists. In some examples the method does not require that the subject exercise, and as such, the subject may be sedentary (such as bedridden or in a wheelchair).

Abstract: This application relates to methods of treating and ameliorating fibrosis, such as fibrosis of the pancreas. In particular, the application relates to methods of using a vitamin D receptor agonist (such as vitamin D, vitamin D analogs, vitamin D precursors, and vitamin D receptor agonists precursors) for the treatment of pancreatic fibrosis.

Abstract: Provided herein is, inter alia, methods and compositions useful in therapeutic interrogation of complex physiologic pathways by massively parallel and permissive transcriptional screening. Thus, methods and compositions are provided herein that are useful for high-throughput functional analysis of complex, transcriptionally regulated physiological pathways. While examples are provided relating to nuclear receptors, the methods and composition can be generalized and applied to any class of transcription factor or any class of gene product that can regulate the activity of transcription. For example, in addition to nuclear receptors, the methods and compositions provided herein are generally applicable to all known transcription factors and any gene encoded product that modulates said transcription factor activity. Moreover, data obtained through the methods provided herein are directly comparable thereby facilitating high-throughput functional analysis.

Abstract: This disclosure concerns the use of agonists of AMP-activated protein kinase (AMPK) for improving exercise and modifying energy metabolism in a subject. The disclosure also relates to a combination of AMPK and peroxisome proliferator-activated receptor (PPAR) ? agonists for improving exercise performance in a subject, methods for identifying substance-enhanced exercise performance in a subject, and methods for identifying compounds that affect the interaction of PPAR? with exercise-induced kinases.

Abstract: This application relates to methods of treating, preventing, and ameliorating fibrosis, such as fibrosis of the liver. In particular, the application relates to methods of using a vitamin D receptor agonist (such as vitamin D, vitamin D analogs, vitamin D precursors, and vitamin D receptor agonists precursors) for the treatment of liver fibrosis. Also disclosed are methods for screening for agents that treat, prevent, and ameliorate fibrosis.

Abstract: This application relates to methods of treating, preventing, and ameliorating fibrosis, such as fibrosis of the liver, kidney, or pancreas. In particular, the application relates to methods of using a vitamin D receptor agonist (such as vitamin D, vitamin D analogs, vitamin D precursors, and vitamin D receptor agonists precursors) for the treatment of fibrosis. Also disclosed are methods for screening for agents that treat, prevent, and ameliorate fibrosis.

Abstract: Disclosed herein are methods for enhancing one or more effects of exercise in a subject by administering a PPAR? agonist (e.g., GW1516) to the subject in combination with an exercise program. Also disclosed are gene expression profiles unique to the combination of agonist-induced PPAR? activation and exercise. Such profiles are useful, at least, in methods for identifying the use of performance-enhancing drugs in exercised subjects (such as, professional or athletes). Direct interactions between PPAR? and exercised-induced kinases (e.g., AMPK or its subunits, AMPK ?1 and/or AMPK ?2) also are disclosed. Such protein-protein interactions provide new targets for identification of useful compounds.