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 releasably locks at least one rail in its channel. A mounting bracket is attached rearward of one tray portion.

Abstract: The present disclosure provides compositions that include a nanoparticle and a compound that increases the biological activity of the vitamin D receptor (VDR) (e.g., a VDR agonist), and methods of using such compounds to increase retention or storage of vitamin A, vitamin D, and/or lipids by a cell, such as an epithelial or stellate cell. Such methods can be used to treat or prevent fibrosis.

Abstract: Provided herein are methods and kits for increasing cardiac contraction, increasing mitochondrial activity, and/or increasing oxphos activity. Such methods include use of therapeutically effective amounts of one or more agents that increases estrogen-related receptor (ERR) ? activity and one or more agents that increases ERR? activity. In some examples, the method further includes administering a therapeutically effective amount of one or more agents that increases mitofusin 1 (Mfn1) activity.

Abstract: Disclosed are embodiments of a method of treating or preventing latent autoimmune diabetes of adults (LADA) in a subject. Such embodiments include administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or farnesoid X receptor (FXR) agonist compounds, thereby activating FXR receptors in the intestines, and treating or preventing latent autoimmune diabetes of adults (LADA) in the subject.

Abstract: The present disclosure provides FGF1 mutant proteins having one or more mutations in the heparin binding domain. Such mutants may also have an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the 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. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.

Abstract: A path of travel used by an autopilot operation system for auto-guidance of a mobile machine is defined, transparently to a human operator, in response to the human operator engaging and disengaging operation of an implement coupled with the mobile machine. The auto-guidance of the mobile machine is activated, transparently to the human operator, in response to the human operator engaging the implement a second time.

Abstract: Auto-guidance of a mobile machine is provided that does not require a graphical user interface display. Human interactions with the auto-guidance system of a mobile machine are performed solely with one or more electromechanical switches of the auto-guidance system while the mobile machine is operating. A first point for auto-guidance of a mobile machine is set by an auto-guidance system in response to a first electromechanical switch input. A second point for auto-guidance of the mobile machine is set by the auto-guidance system in response to a second electromechanical switch input after movement of the mobile machine from the first point. The auto-guidance system activates auto-guidance of the mobile machine along a path defined by the first point and the second point. The setting of the first point, the setting of the second point, and the activating are performed by one or more hardware processors.

Abstract: The present disclosure provides FGF1 mutant proteins having one or more mutations in the heparin binding domain. Such mutants may also have an N-terminal deletion, point mutation(s), or combinations thereof. In some examples, the 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. The disclosed FGF1 mutants can reduce blood glucose in a mammal, and in some examples are used to treat a metabolic disorder.

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

Abstract: Provided herein are compounds of formula (I) useful for the treatment of PPAR-delta related diseases (e.g. mitochondrial diseases, muscular diseases, vascular diseases, demyelinating diseases and metabolic diseases).

Abstract: Provided herein are compounds of Formula (I) and compositions useful in increasing PPARS activity. The compounds and compositions provided herein are useful for the treatment of PPARS related diseases (e.g., muscular diseases, vascular disease, demyelinating disease, and metabolic diseases).

Abstract: The present disclosure provides FGF2 mutant proteins, such as those having an N-terminal deletion, point mutation(s), or combinations thereof, which can reduce blood glucose in a mammal. Thus, the disclosed mutant FGF2 proteins can be used to treat one or more metabolic diseases. In some examples, mutant FGF2 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, for example to treat a metabolic disorder are also provided.

Abstract: Provided herein are deuterated compounds and compositions useful in increasing PPAR? activity. The compounds and compositions provided herein are useful for the treatment of PPAR? related diseases (e.g., muscular diseases, vascular disease, demyelinating disease, and metabolic diseases).

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: A method for creating a compound media stream includes obtaining a first media segment, obtaining a first matching criterion, and automatically associating the first media segment with an existing media stream to produce the compound media stream.

Abstract: The invention relates to a buggy comprising an upper sliding frame and a lower sliding frame to which the front wheels are attached. In the upright driving position of the buggy, viewed in the side view, the upper sliding frame and the lower sliding frame are approximately aligned with one another. There is also a rear frame to which the rear wheels are attached. In the driving position, the buggy, viewed from the side, is oriented at an angle to the sliding frames, and the buggy can be collapsed about joints from the driving position into a transport position. Joint units, to which the respective end of a strut of the upper sliding frame facing the joint units and the respective end of a strut of the rear frame facing the joint units, are attached so as to be pivotable about joint axes, which are parallel to one another.

Abstract: Novel compounds having a formula embodiments of a method of making the same, and of a composition comprising them are disclosed herein. Also disclosed are embodiments of a method of treating or preventing a metabolic disorder in a subject, comprising administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and treating or preventing a metabolic disorder in the subject. Additionally disclosed are embodiments of a method of treating or preventing inflammation in an intestinal region of a subject, comprising administering to the subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and thereby treating or preventing inflammation in the intestinal region of the subject.

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

Abstract: Novel FXR agonists are disclosed, embodiments of a method of making the same, and of a composition comprising them are disclosed herein. Also disclosed are embodiments of a method of treating or preventing a metabolic disorder in a subject, comprising administering to a subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and treating or preventing a metabolic disorder in the subject. Additionally disclosed are embodiments of a method of treating or preventing inflammation in an intestinal region of a subject, comprising administering to the subject (e.g., via the gastrointestinal tract) a therapeutically effective amount of one or more of the disclosed compounds, thereby activating FXR receptors in the intestines, and thereby treating or preventing inflammation in the intestinal region of the subject.

Abstract: An electronic device caddy includes a first tray portion an end cage and a second tray portion also including an end cage. A passive sound amplifier is associated with one end cage. A locking mechanism is also featured. A mounting bracket is attached rearward of one tray portion.