Abstract: Various shaped abrasive particles are disclosed. Each shaped abrasive particle includes a body having at least one major surface and a side surface extending from the major surface.

Abstract: Provided are methods for treating diseases, disorders, and conditions associated with undesirable cellular proliferation in subjects in need thereof. In some embodiments, the methods include administering to a subject in need thereof a therapeutically effective amount of a composition comprising, consisting essentially of, or consisting of a chemotherapeutic agent and a short chain ceramide. Also provided are methods for increasing total ceramide levels in cells, for increasing long chain ceramide to a very long chain ceramide ratios in cells, methods for enhancing apoptosis of cells, for prognosing subjects with diseases, disorders, and conditions associated with undesirable cellular proliferation with respect to treatments, for increasing sensitivities of drug-resistant tumor and/or cancer cells to chemotherapeutics, and compositions that have one or more short chain ceramides and one or more chemotherapeutically active agents.

Abstract: Provided are methods for preventing and/or reducing weight gain in subjects. In some embodiments, the methods include administering an effective amount of a composition that includes a long chain fatty acid of at least 22 carbons and/or a derivative thereof to prevent and/or reduce weight gain in the subject. In some embodiments, the long chain fatty acid is a monounsaturated omega 9 fatty acid, which in some embodiments is nervonic acid or a derivative thereof. Also provided are methods for preventing and/or reducing the development of obesity in subjects, for inhibiting reduction of very-long chain sphingolipids in subjects, for increasing content of one or more ceramides while simultaneously decreasing content of one or more C20-C26 ceramides in subjects, and for reducing blood glucose levels resulting from consumption of high fat diets in subjects.

Abstract: Use of dhS1P and/or PhotoImmunoNanoTherapy as a therapeutic agent is described. Administration of therapeutically effective amounts of dhS1P decrease the number of Myeloid Derived Suppressor Cells and immune suppression in cancer patients. Administration of therapeutically effective amounts of dhS1P can be used as an adjuvant to conventional cancer therapies including immunotherapies. Therapeutic results can be achieved by directly administering dhS1P and/or by indirectly increasing the amount of dhS1P at the tumor site. The therapy permits the patient's immune system to recognize and eliminate cancer cells reducing tumor size and extending patient survival.

Abstract: Use of dhS1P and/or PhotoImmunoNanoTherapy as a therapeutic agent is described. Administration of therapeutically effective amounts of dhS1P decrease the number of Myeloid Derived Suppressor Cells and immune suppression in cancer patients. Administration of therapeutically effective amounts of dhS1P can be used as an adjuvant to conventional cancer therapies including immunotherapies. Therapeutic results can be achieved by directly administering dhS1P and/or by indirectly increasing the amount of dhS1P at the tumor site. The therapy permits the patient's immune system to recognize and eliminate cancer cells reducing tumor size and extending patient survival.

Abstract: Diabetic retinopathy is a debilitating complication of diabetes and a leading cause of vision loss, however the fundamental mechanisms contributing to vision loss remain undefined. Several novel observations are described: 1) diabetic retinas demonstrate decreased total ceramide levels; 2) with a concomitant increase in glucosylceramides; 3) which mediates decreased insulin receptor signaling and; 4) cell death in vitro and in vivo. Inhibition of this dysfunctional glycosphingolipid metabolism restores insulin sensitivity. Moreover, elevation in diglycerides and reduction in concentrations of phosphatidic acid or ceramide-1-phosphate also contribute to diabetic complications and insulin resistance. The mechanism responsible for dysfunctional lipid metabolism in diabetic tissues involves reduced caveloin-1-expression within structured membrane microdomains and suggest another target for molecular and pharmacological intervention.