A pharmaceutical product containing β2-microglobulin or a functional variant thereof as an active ingredient in the form of liposomes is provided. The product can increase the concentration of β2-microglobulin in the blood, and can also restore a normal HC/β2-microglobulin molar ratio within membrane MHC-I complexes, or prevent a β2-microglobulin deficit from occurring in the MHC-I complexes, of patients suffering from autoimmune diseases. Methods of treating patients with the pharmaceutical product are also presented.

The invention pertains to the use of a specific biomarker of elastin degradation (desmosine) that measures the extent and progression of chronic obstructive pulmonary disease (COPD). In addition to potentially serving as a screening procedure for COPD, it provides a real-time measure of COPD drug efficacy and may therefore supersede the use of less sensitive tests such as pulmonary function studies and computed tomography. Equally important, the current invention constitutes a marked improvement for measuring desmosine in tissues and body fluids by greatly shortening the time for detection of this molecule in liquid chromatography-tandem mass spectrometry (LC-MS-MS) assays that are the gold standard for such measurements. Unlike previous methods, the invention allows for the use of LC-MS-MS without modification, so the method can be applied to any laboratory that uses this equipment for other measurements. This would include forensic facilities that need to determine if undiagnosed COPD played a role in the loss of life.

The invention relates to a SERS method for analyzing a biological sample, the method comprising the following step of: a. obtaining a biological sample which is viscous biofluid, b. depositing at least one droplet of the biological sample onto a microscope slide, and drying the droplet, c. depositing a drop of an aqueous dispersion of metallic nanoparticles above the droplet dried in step b), to have a dense distribution of nanoparticles on the surface of the dried droplet and to obtain a SERS-activated biological sample, d. drying the SERS-activated biological sample, e. irradiating the SERS-activated biological sample using a light source to obtain a SERS spectrum, and f. collecting the SERS spectrum.

The invention relates to methods of treating fibrosis and inflammatory bowel disease. In one embodiment, the present invention treats gut inflammation by administering a therapeutically effective dosage of TL1A inhibitors and/or DR3 inhibitors to an individual. In another embodiment, the present invention provides a method of reversing tissue fibrosis in an individual by inhibiting TL1A-DR3 signaling function.

The present invention relates to the field of protein purification and relates in particular to novel proteins that bind to the soluble part of fibroblast growth factor receptor 3 (sFGFR3). The invention further relates to fusion proteins comprising novel proteins that bind to sFGFR3. In addition, the invention relates to affinity matrices comprising the sFGFR3 binding proteins of the invention. The invention also relates to a use of these sFGFR3 binding proteins or affinity matrices for affinity purification of sFGFR3 nd to methods of affinity purification of sFGFR3 using the sFGFR3 binding proteins of the invention. Further uses relate to analytical methods for the determination of SFGFR3 in liquids.

The invention belongs to the technical field of collagen detection, and in particular relates to a peptide probe for the specific detection of pathological collagen in tissues, the preparation methods and applications. The peptide probe disclosed in this invention comprises a peptide sequence (Gly-Hyp-Pro).sub.n and a signal molecule modified at the N-terminal of the peptide sequence (Gly-Hyp-Pro).sub.n. The peptide sequence (Gly-Hyp-Pro).sub.n can maintain a stable single-stranded conformation without introducing other components, and will not form a trimer state at all. After the N-terminal of the peptide sequence is connected with a signal molecule, it can be used as a peptide probe for the detection of pathological collagen. The preparation method of the peptide probe is simple. Compared with the existing peptide (GPO, GPP or GOO) probe, it can continuously maintain 100% single-stranded structure, and the concentration of the single-chain probe can be accurately quantified. Moreover, this peptide probe can recognize pathological collagen in tissues of diseases such as arthritis, which has wide prospects of application in fields such as early diagnosis and efficacy evaluation of collagen-related diseases.

Methods, reagents, and kits for assaying for arylsulfatase A activity for diagnosing conditions associated with arylsulfatase A deficiency, such as multiple sulfatase deficiency (MSD) and metachromatic leukodystrophy (MILD).

The present invention discloses a novel therapeutic intervention for osteoporosis. The present invention discloses that Interleukin-3 (IL-3) can be utilized as a therapeutic intervention against osteoporosis and for regulating bone homeostasis. The present invention also provides a method for determining the pre-disposition of a subject for osteoporosis by measuring the RANKL/OPG level.

The inventors initially participated to the identification of LPIN1 mutations as a cause for massive rhabdomyolysis episodes in children, triggered by febrile illness. The inventors have suggested that TLR9 antagonists would be suitable for the treatment of rhabdomyolysis (WO2017085115). The inventors thus treated 2 patients with lipin-1 disease by a TRL9 antagonist (hydroxychloroquine). They showed that the accumulation of mtDNA in plasma of the two patients before treatment decreases under treatment. When the treatment was stopped, the accumulation of mtDNA reappeared, then normalized when treatment was resumed. Accordingly, the present invention relates to a method for determining whether a patient suffering from rhabdomyolysis achieves a response with a TLR9 antagonist comprising determining the amount of mitochondrial DNA (mtDNA) in a blood sample obtained from the patient (e.g. by PCR).

A method for monitoring a treatment of a subject having a musculoskeletal disorder is provided. The method includes measuring a first expression level of at least two biomarkers at a treatment site prior to the treatment and measuring a second expression level of the at least two biomarkers at the treatment site after the treatment begins. The method further includes comparing the first expression level of the at least two biomarkers prior to the treatment to the second expression level of the at least two biomarkers post treatment and continuing the treatment, altering the treatment or stopping the treatment based on the comparison. A method of treating a musculoskeletal disorder in a subject is also provided. The method includes removing a aggrecan-hyaluronan matrix from a treatment site in the subject.