A method for treating an individual at risk for a complement-associated disorder is provided, the method including: (a) obtaining a sample of a body fluid from the individual; (b) measuring a complement activation level in the sample via a point-of-care lateral flow immunoassay; (c) correlating the complement activation level in the sample to a risk of a complement-associated disorder by comparing the complement activation level in the sample to a reference level in a control, wherein a deviation in complement activation level in the sample compared to the reference level in the control indicates the individual is at risk for a complement-associated disorder; (d) selecting a treatment for the individual, based on the correlating of step (c); and (e) treating the individual with the treatment selected in accordance with step (d). Lateral flow immunoassays for the qualitative and quantitative point-of-care detection of complement activation and a method of monitoring an individual suffering from a complement-associated disorder are also provided herein.

Disclosed is a method for assisting prediction of exacerbation of respiratory infection, comprising measuring a biomarker in a specimen collected from a subject suffering from a respiratory infection or a subject suspected of having a respiratory infection, wherein the biomarker is at least one selected from the group consisting of IFN3, CCL17, CXCL11, IP-10, IL-6 and CXCL9, and a measured value of the biomarker is used as an index to predict exacerbation of the respiratory infection.

The present invention is related to novel methods for categorizing and treating a population of subjects having cystic fibrosis (CF) and who are at risk of severe pulmonary exacerbation comprising detecting the expression levels of genes in a gene panel consisting of TLR2, ADAM9, PLXND1, CD163, CD36, CD64, CSPG2, IL32, HPSE, and HCA112 and aggressively treating the subject when the expression levels of the genes from the gene panel predicts the subject is at risk for severe pulmonary exacerbation.

The present invention relates to the biomarkers for predicting the clinical response to anti-LPS immunoglobulin treatments in patients in need thereof. In particular, the invention provides methods for predicting the clinical response to an anti-LPS immunoglobulin treatment in a patient in need thereof, said method comprising the steps of evaluating the expression of a predictive biomarker selected from the group consisting of CD14, CD68, TLR4, TLR7, IL6, IL8, IL10, IFN-alpha, IGF1, CXCL1, CXCL9, CXCL10, RAGE, GDNF, BCHE, and combination thereof, in said patient.

The present invention features compositions and methods for enhancing an anti-tumor response by administering an OX40 agonist (e.g., an anti-OX40 antibody) and/or an anti-CTLA4 antibody (e.g., a CTLA4-blocking antibody) in combination with a cancer therapy.

The present invention is related to novel methods for categorizing and treating a population of subjects that are at risk for increased pulmonary exacerbation and disease progression.

There is disclosed a pharmaceutical composition and method for treating sepsis, including septic shock and ARDS (acute respiratory distress syndrome), comprising administering an effective amount of a HMG1 antagonist. There is further disclosed a diagnostic method for monitoring the severity or potential lethality of sepsis or septic shock, comprising measuring the serum concentration of HMG1 in a patient exhibiting or at risk of exhibiting sepsis or septic shock symptoms. Lastly, there is disclosed a pharmaceutical composition and method for effecting weight loss or treating obesity, comprising administering an effective amount of HMG1 or a therapeutically active HMG1 fragment.

The technology described herein is directed to methods of producing or differentiating AT1 cells, and AT1 cells made by the methods described herein.

The present disclosure relates to a method of treating a subject suffering from respiratory distress or preventing respiratory distress in a subject at risk thereof with an IL-33 axis antagonist, to a method of determining whether such a subject will respond to treatment with an IL-33 axis antagonist, and to a method of selecting a subject for treatment with an IL-33 axis antagonist, by determining whether the level of IL-33/sST2 in a sample obtained from the subject is greater than or equal to a given reference level. Uses corresponding to said methods are also provided.

A pharmaceutical composition for administering directly to the pulmonary tract of a subject includes a salt of triiodothyronine and a pharmaceutically acceptable buffer, adjusted to a pH of 5.5-8.5. The composition can be administered prophylactically or therapeutically to a subject to treat lung inflammation or pulmonary edema.