Methods for the treatment of a respiratory infection, for the prevention of worsening of symptoms associated with the infection, and for reducing the lethality of the infection such as but not limited to respiratory infections caused by a coronavirus. The present disclosure provides specific gaseous nitric oxide (NO) dosing regimens optionally paired with the monitoring of toxicology outcomes so as to enable the use of effective NO doses for treatment purposes. The present invention also discloses air circulation systems featuring NO for helping to prevent respiratory infections.

The present disclosure provides methods and kits for detecting Group A Streptococcus in biological samples. More particularly, the present disclosure provides methods for enhancing the specificity and sensitivity of Group A Streptococcus immunoassays by including N-propionyl-D-glucosamine, 2-N-butanoyl-D-glucosamide, Bis-(2-(D-2-deoxy-glucosaminyl))-PEG3-amide, m-PEG4-glucosamine, m-PEG6-glucosamine, or m-PEG10-glucosamine. The methods and kits disclosed herein are thus useful for reliable and early diagnosis of streptococcal infections in a subject.

Disclosed is a method for selecting a cancer treatment regimen for a subject.

The present invention relates to the use of receptor tyrosine kinase (RTK) oligomers as markers of RTK activation and signalling. Methods are described based upon determining the presence of RTK oligomers and/or determining the nanometre spatial separation between RTK molecules assembled as RTK oligomers at the cell surface. Such methods are directed to the monitoring of RTK activation in cells and the detection of mutations in RTKs. Methods are also described for determining prognosis for subjects having diseases characterised by aberrant RTK activation and for selecting subjects for treatment with RTK inhibitors.

A method of predicting the likelihood of success of a gene therapy procedure includes inducing DNA damage in a cell sample from an individual. The ability of the individual's cells in the sample to repair the DNA damage is then assessed to determine whether the individual could tolerate DNA damage caused by a gene therapy vector. In preferred embodiments, the ability of the individual's cells to repair DNA damage is assessed by detecting, and monitoring the subsequent disappearance of, a marker of DNA damage repair (such as gamma H2AX or phosphorylated 53BP1) in the sample.

A method for detecting and quantifying of the frequency of T cells to multiple antigenic peptide epitopes comprising: measuring intracellular Ca2+ signaling in individual T cells that are labeled with Ca2+ sensitive fluorophore; wherein said T cells are placed on the glass bottom of a well-covered with antibodies or other capturing proteins specific for non-stimulatory T cells' surface receptors and wherein a peptide antigens are injected into the well and the peptide binds to MHC molecules on the T-cell surface, wherein an increase in the intracellular concentration of Ca2+ in responding T cells leads to rise in intracellular fluorescence that is detected by fluorescent microscope and wherein the response rate of said detected fluorescence can be utilized to determine the quantity of responding T cells and the efficiency of said cells.

There is described herein a method of prognosing endocrine-only treatment in a subject with breast cancer, the method comprising: a) providing a tumor sample of the breast cancer; b) determining the expression level of at least 40 of the genes listed in Table 4 in the tumor sample; c) comparing said expression levels to a reference expression level of the group of genes from control samples from a cohort of subjects; and d) determining the residual risk associated with the breast cancer; wherein a statistically significant difference or similarity in the expression of the group of genes compared to the reference expression level corresponds to a residual risk associated with breast cancer.

Provided herein are methods and articles of manufacture for use with cell therapy for the treatment of diseases or conditions, e.g., cancer, including for predicting and treating a toxicity. In some embodiments, the toxicity is related to cytokine release syndrome (CRS). The methods generally involve assessing a change in a factor indicative of tumor burden prior to administration of a cell therapy in a subject that is associated with and/or correlate to a risk of developing toxicity. In some aspects, the methods can be used to determine if the subject is at risk or likely at risk for developing a toxicity following administration of the cell therapy. Also provided are methods for treating a subject having a disease or condition, in some cases involving administration of the cell therapy, based on assessment of risk of developing a toxicity following administration of the therapy. Also provided herein are reagents and kits for performing the methods.

Methods and kits for predicting infusion reaction risk and antibody-mediated loss of response during intravenous PEGylated uricase therapy in gout patients is provided. Routine SUA monitoring can be used to identify patients receiving PEGylated uricase who may no longer benefit from treatment and who are at greater risk for infusion reactions.

The present invention relates to developing customized therapies for a disease or condition in a subject. In particular, the present invention relates to aptamer-based compositions and methods for identifying, modulating and monitoring drug targets in individual with a disease or condition, and further composition and methods for identifying and selecting protein targets for drug development.