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.

Disclosed herein is a method of detecting the presence of skin UV damage based on molecular risk factors. In some instances, also described herein is a method of determining the progression of UV damage based on the molecular risk factors.

A method for detection or monitoring status of traumatic brain injury (TBI) and/or spinal cord injury (SCI) in a subject is provided. In one embodiment, the method comprises contacting a specimen of bodily fluid obtained from the subject with reagents for assaying for a marker of TBI selected from aldolase C (ALDOC) and brain lipid binding protein (BLBP/FABP7), or a trauma-specific break down product (BDP) of ALDOC or BLBP/FABP7. The method further comprises measuring the amount of marker present in the specimen as compared to a control sample, and determining the presence of TBI or SCI when an elevated amount of marker is present in the specimen compared to the control sample. Optionally, the method further comprises measuring the amount of glutamine synthetase (GS), astrocytic phosphoprotein PEA-15 (PEA15), B-crystallin (CRYAB/HSP27), a trauma-specific proteolytic cleavage product of ALDOC, GS, PEA15, or CRYAB, or any combination of two or more thereof.

Proteins that are differentially expressed or elevated in tissue and biofluids after central nervous system injuries are described. Elevated or reduced levels of the proteins, alone or in various combinations or ratios, can be used to assess severity of central nervous system injury (CNS injury) including traumatic brain injury (TBI), traumatic spinal cord injury (SCI) and chronic traumatic encephalopathy (CTE). Time course measurements post CNS-injury of these proteins can be used to monitor progress or recovery over periods up to several months. Differentiation of acute, subacute and chronic injury can be diagnosed by comparing the protein levels in CNS-injury patients at days 1-3, day 4-10 with levels at day 30-180 in comparison with normal controls.

The present invention is drawn to a new diagnosis method and a calculator for predicting the risk of developing a breast late effect (BLE), which is defined as atrophic skin, telangiectasia, induration (fibrosis), necrosis or ulceration, in a subject after radiotherapy (RT), by using Radiation Induced late effect using T-Lymphocyte Apoptosis (RILA) and clinical parameters. The invention is also drawn to diagnosis kits for the implementation of the method and a nomogram.

The present disclosure is directed to methods (e.g., in vitro methods) for use of nicotinamide phosphoribosyltransferase (NAMPT) as a biomarker in radiation-induced lung injury (RILI). Provided herein is an in vitro method for the diagnosis, prognosis, and/or monitoring of RILI in a human subject by providing a tissue or plasma sample from the subject and detecting the level of NAMPT therein, wherein a higher level of NAMPT in the tissue or plasma sample from the subject compared to a healthy control or a reference value is indicative for the presence of RILI in the subject. Further provided herein is a method of detecting NAMPT in a human subject by obtaining a biological sample from the subject, detecting the presence of NAMPT in the sample by contacting the sample with a capture agent that specifically binds NAMPT, and detecting binding between NAMPT and the capture agent.

A method for detection or monitoring status of traumatic brain injury (TBI) or spinal cord injury (SCI) in a subject is provided. In one embodiment, the method comprises contacting a specimen of bodily fluid obtained from the subject with reagents for assaying for a marker of TBI selected from aldolase C (ALDOC) and brain lipid binding protein (BLBP), or a trauma-specific break down product (BDP) of ALDOC or BLBP. The method further comprises measuring the amount of marker present in the specimen as compared to a control sample, and determining the presence of TBI or SCI when an elevated amount of marker is present in the specimen compared to the control sample. The method can comprises measuring the amount of glutamine synthetase (GS), astrocytic phosphoprotein PEA-15 (PEA15), B-crystallin (CRYAB/HSP27), a cleavage product of ALDOC, GS, PEA15, or CRYAB, or a combination of two or more thereof.

The present invention relates to methods and kits to assess an absorbed dose of ionizing radiation and/or the severity of tissue injury from radiation in a patient. The invention also relates to algorithms used to calculate an absorbed dose of radiation based on biomarker measurements of a plurality of biomarkers that are altered relative to a normal control in the event of radiation exposure.

A high throughput automated assay platform for temporal image processing of cell growth and colony formation before and after radiation therapy treatments. The platform is designed to compute and monitor a therapeutic protocol by measuring sensitivity of cell growth to treatment based on a radiation therapy protocol. The platform is designed to detect relationships between the temporal images being tracked to colony formation behaviour.

Known or suspected traumatic brain injuries may be treated therapeutically by administering a therapeutically effective dose of resibufogenin. A preferred method for determining if a patient has a traumatic brain injury includes obtaining a body specimen from the patient, determining the concentration of marinobufagenin in the body specimen, comparing the concentration of marinobufagenin to the concentration in such body specimens in normal patients, and if the marinobufagenin concentration is substantially above the concentration of a normal patient, concluding traumatic brain injury exists. In a preferred embodiment, a substantial elevation is deemed to be an increase of about 30 percent above the marinobufagenin concentration of a normal patient. The body specimen may be blood, urine, or cerebrospinal fluid. If a substantial elevation is deemed to exist, the magnitude of the departure from the concentration of a normal patient may be employed in determining the timing and nature of treatment provided to the patient. The method may be repeated at predetermined intervals to monitor changes in the marinobufagenin with time.