Methods and materials are disclosed for evaluating head brain injuries that do not involve blood loss or skull fractures, such as possible concussions. These methods and materials involve bioreagents (such as monoclonal antibodies, single-stranded DNA or RNA, etc.) affixed to computer-readable devices handled by electronic readers that can interact with portable computers (such as laptops, pads or tablets, smart phones, etc.). The bioreagents will detect the presence and concentration of at least two metabolites that are released by mitochondria in response to cellular damage. Additional bioreagents may be included, for detecting and quantifying other damage-associated molecular patterns (DAMP's). When used along with cognitive, reasoning, and/or response tests, this type of analysis can help non-physicians assess the severity of, and proper responses to, head traumas that otherwise are difficult or impossible to reliably evaluate.

The present disclosure provides diagnostic methods useful for predicting a patient's response to alvocidib and guiding a physician decision to administer alvocidib to the patient.

The present invention relates to a method for delivering exogenous mitochondria into cells and, more specifically, to a method for efficiently delivering, into the cytoplasm of target cells to be injected, mitochondria isolated from donor cells.

The present invention provides methods of predicting cell sensitivity or resistance to a therapeutic agent.

The present invention relates to methods of determining cancer cell sensitivity to treatment by correlating the pattern of sensitivity of the cell to a panel of BH3 domain peptides. The invention also provides a method applying an algorithm to said pattern to predict therapeutic efficacy and of monitoring the shift in cell sensitivity to a therapeutic during treatment.

The present disclosure provides diagnostic methods useful for predicting a patient's response to alvocidib and guiding a physician decision to administer alvocidib to the patient.

The present disclosure describes series pH-activable fluorescent probes based on a single BODIPY scaffold selectively targeting lysosomal, mitochondrial, and nucleus. The divergent cell organelle targeting was achieved by synthesizing pH-activable fluorescent probes with differential fluorescence profiles arising due to the presence of a unique functional group in the scaffold. We discovered that the functional group transformation in the same scaffold influences the localization ability of pH-activable fluorescent probes in cell organelle. The development of pH-activable fluorescent probes that target lysosomes and mitochondria organelles in live and fixed primary mouse microglial cells warrants future use in disease-specific biological models.

The present invention relates to a method for screening an activator of mitochondrial activity by using gypenoside-treated cells, to a composition for screening an activator of mitochondrial activity, comprising the gypenoside, and to a kit comprising the composition. By using the method for screening an activator of mitochondrial activity of the present invention, it is possible to effectively discover a preparation which can substantially promote the mitochondrial activity, and thus the method is expected to be widely used in developing a therapeutic agent for diseases caused by mitochondrial activity inhibition.

The present disclosure is generally directed to profiling peptides, compositions, and kits, as well as methods of use thereof. The profiling peptides comprise an Mcl-1 binding domain, and optionally a cellular uptake moiety. The methods of using such profiling peptides include predicting sensitivity of a cancer, selecting a treatment, treating a cancer, producing a sensitivity profile, and the like.

Compositions and methods for treatment of mitochondrial respiratory chain dysfunction and other mitochondrial disorders are provided. Also disclosed are a number of screening assays having utility for the identification of agents which modulate the phenotype associated with mitochondrial respiratory chain dysfunction.