Computational and functional analysis identified the neuropeptide receptor Nmur1 as selectively expressed on Type 2 innate lymphoid cells (ILC2s). While both IL-33 and IL-25 promote ILC activation in vivo, IL-33 induces robust ILC proliferation, whereas ILCs activated with IL-25 do not proliferate as robustly and up-regulate Nmur1 expression. Treatment with neuromedin U (NMU), the neuropeptide ligand of Nmur1, had little effect on its own. Co-administration of IL-25 with NMU, however, dramatically amplified allergic lung inflammation and induced the proliferation and expansion of specific ILC2 subsets, characterized by a molecular signature unique to pro-inflammatory ILC2s. The results demonstrate that Nmur1 signaling strongly modulates IL-25-mediated ILC2 responses, resulting in highly proliferative pro-inflammatory ILCs, and highlights the importance of neuro-immune crosstalk in allergic inflammatory responses at mucosal surfaces.

Described herein are improvements relating to IGF-1 analysis, adjustment and disease management of non-neurological and/or neurological conditions. More specifically, methods relating to the clinical application of cyclic glycine-proline (cGP) biomarker for prediction of risk and recovery of non-neurological and/or neurological conditions with IGF-1 dysfunction and the use of a cGP containing organic or plant based material such as concentrated extract of blackcurrant anthocyanins (BCA) for the treatment of same. The methods more accurately measure IGF-1 function in vivo indirectly using cGP and cGP/IGF-1 ratio along with a means to adjust cGP and cGP/IGF-1 ratio (and hence active IGF-1 concentration), and specific treatment methods for individuals with a lower or reduction of cGP level relative to a standard set of baseline data.

Peptides useful in determining the presence of autoantibodies in patients suffering from rheumatoid arthritis are disclosed.

Provided are a noninvasive measurement of cell signals and a method thereof, wherein the measurement method can ascertain cell proliferation and differentiation states using MRS and can enable cells to be reused so that cell states can be evaluated with improved reproducibility and reliability. And since the cell signals are noninvasively measured using the MRS, the corresponding cells can be reused so that the cost and time needed for one experiment can be remarkably reduced.

Peptides useful in determining the presence of autoantibodies in patients suffering from rheumatoid arthritis are disclosed.

A method evaluates a quality of a dephosphorylation reagent, the method including the steps of: providing a dephosphorylation reagent containing an alkaline phosphatase and a peptide fragment derived from the alkaline phosphatase; and evaluating the dephosphorylation reagent as having a high quality if a content ratio of the peptide fragment to the alkaline phosphatase is a predetermined reference value or less.

Described herein are improvements relating to IGF-1 function analysis, adjustment and its application in disease management of non-neurological and/or neurological conditions. More specifically, methods relating to the clinical application of cyclic glycine-proline (cGP) and/or cGP/IGF-1 molar ratio as the plasma biomarker for prediction of risk and recovery of non-neurological and/or neurological conditions with IGF-1 dysfunction and the use of a cGP containing animal, marine or fungal based material such as concentrate/extract of hydrolysed bovine collagen and marine collagen, mushroom and seaweed along with plant-based cGPMAX for the treatment of same. The methods more accurately measure IGF-1 function in vivo indirectly using cGP and cGP/IGF-1 molar ratio along with a means to adjust and normalise cGP and cGP/IGF-1 molar ratio (and hence active IGF-1 concentration), and specific treatment methods for individuals with a lower or reduction of cGP level relative to a standard set of baseline data. Supplementation of bovine collagen formulated cGPMAX effectively improved the sensory function in patients with diabetic neuropathy.

Provided are methods for identifying OP-adducted biomarkers of OP exposure as well as compounds containing OPs that can provide OP adducts and compounds of Formula 1 for eliciting antibodies that specifically and selectively bind to the OP adducts, wherein the Formula 1 compounds have the structure of OP-Peptide-Linker-CP, wherein CP is a carrier protein, OP represents a structure corresponding to that of a reactive organic phosphorous compound covalently modifying a tyrosine residue hydroxyl group of the peptide of Formula I and the other variable groups are as described herein.

The present disclosure provides organophosphorous (OP) compounds of Formula (I), Formula (II) and Formula (III):
OP-Peptide-Linker-CP(I),
OP-Peptide-Linker(II); and ##STR00001## wherein OP is ##STR00002##
including that structure corresponding to a reactive organophosphorous reagent, nerve agent or pesticide, or a pesticide PS to PO metabolite; P is the S.sub.p or R.sub.p stereoisomer; X is oxygen, sulfur, selenium or imino; R and R are as described; Peptide is a sequence of amino acids containing a serine, threonine or tyrosine to which the OP is attached, wherein the total number of amino acids is between 7 and 41; Linker is an amino acid or is derived from another bifunctional reagent capable of covalently attaching an OP-peptide to a CP; and CP is a carrier protein used to display haptens for antibody generation. The disclosure also provides methods for generating monoclonal or polyclonal antibodies specific for an OP-Peptide of a compound of Formula (I) or Formula (II) that can be used to diagnose the presence, identity, and quantity of OP adducts.

A method for assessing a suicidal severity in a depressed patient according to an embodiment includes measuring a concentration of a suicidal behavior prediction biomarker contained in a biological sample of the depressed patient, wherein the suicidal behavior prediction biomarker is one or more markers selected from the group consisting of cortisol, interleukin-1 beta (IL-1), homocysteine, total cholesterol, and folate, and determining a probability of an increased suicidal severity by comparing the measured concentration of the suicidal behavior prediction biomarker with a preset cutoff level thereof.