The present disclosure relates to quantum dot nanoparticles useful for targeting and manipulating mitochondrial function, and to methods of targeting and manipulating mitochondrial function using such quantum dot nanoparticles.

The present disclosure relates to quantum dot nanoparticles useful for targeting and manipulating mitochondrial function, and to methods of targeting and manipulating mitochondrial function using such quantum dot nanoparticles.

The present invention provides compounds and methods for the treatment of LFA-1 mediated diseases. In particular, LFA-1 antagonists are described herein and these antagonists are used in the treatment of LFA-1 mediated diseases. One aspect of the invention provides for diagnosis of an LFA-1 mediated disease and administration of a LFA-1 antagonist, after the patient is diagnosed with a LFA-1 mediated disease. In some embodiments, the LFA-1 mediated diseases treated are dry eye disorders. Also provided herein are methods for identifying compounds which are LFA-1 antagonists.

The present invention provides compounds and methods for the treatment of LFA-1 mediated diseases. In particular, LFA-1 antagonists are described herein and these antagonists are used in the treatment of LFA-1 mediated diseases. One aspect of the invention provides for diagnosis of an LFA-1 mediated disease and administration of a LFA-1 antagonist, after the patient is diagnosed with a LFA-1 mediated disease. In some embodiments, the LFA-1 mediated diseases treated are dry eye disorders. Also provided herein are methods for identifying compounds which are LFA-1 antagonists.

The present invention is directed to a method for treating diabetes. The method comprises administering to a subject in need thereof dapansutrile, or a pharmaceutically acceptable solvate thereof, in an effective amount. Oral administration is a preferred route of administration.

The present invention is directed to a method for treating diabetes. The method comprises administering to a subject in need thereof dapansutrile, or a pharmaceutically acceptable solvate thereof, in an effective amount. Oral administration is a preferred route of administration.

Heart failure with preserved ejection fraction (HFpEF) which results from diastolic dysfunction is a growing epidemiologic problem. However, the pathophysiology of this disease is poorly understood. Our goal is to investigate whether microvessel disease may promote HFpEF. To do so we have used Leptin receptor deficient (Lepr.sup.db/db) female mice as a model of HFpEF and performed a transcriptomic analysis via RNA sequencing of the cardiac vascular fraction of both these mice and their control Lepr.sup.db/+littermates. In Lepr.sup.db/db female mice, end diastolic pressure (EDP) signing diastolic dysfunction is significantly increased from 3 month of age. It is correlated with a cardiac and cardiomayocyte hypertrophy, vascular leakage, endothelial cell activation and leucocyte infiltration. As expected, the RNA sequencing analysis confirmed endothelial dysfunction. Besides, it also revealed a strong increase in several mast cell markers. We confirmed, via histology, an accumulation of mast cells in the heart of Lepr.sup.db/db mice. Importantly, it was associated with increased levels of circulating IgE. Lepr.sup.db/db mice were then treated or not with Cromolyn sodium, an inhibitor of mast cell degranulation. After a month treatment, EDP was significantly reduced in Lepr.sup.db/db mice demonstrating the critical role of mast cell in the development of diastolic dysfunction in diabetic obese mice.

Prooxidative chain-transfer agents for use in the treatment of a malignant tumour disease, or infectious disease. The prooxidative chain-transfer agents are selected from lipophilic thiols, lipophilic trithiocarbonates, lipophilic, aromatic dithioesters, and lipophilic, aromatic thiols. The compounds amplify the prooxidative activity at the target site and are therefore highly efficient and specific for their targets.

The present invention is directed to a method for preventing and/or treating Alzheimer's disease. The method comprises administering to a subject in need thereof an effective amount of dapansutrile. The method reduces neuroinflammation and improves the cognitive functions such as learning and memory processes of the subject. Dapansutrile can be administered to the subject orally at a dose of 100-2000 mg/day for 3 months to 5 years or longer.

The present invention is directed to a method for preventing and/or treating Alzheimer's disease. The method comprises administering to a subject in need thereof an effective amount of dapansutrile. The method reduces neuroinflammation and improves the cognitive functions such as learning and memory processes of the subject. Dapansutrile can be administered to the subject orally at a dose of 100-2000 mg/day for 3 months to 5 years or longer.