The present disclosure relates, in general, human antibodies against human parathyroid hormone receptor 1 (PTH1R) and methods of use of such antibodies in the treatment of cancer, Humoral Hypercalcemia of Malignancy (HHM), or Primary Hyperparathyroidism (PHPT) and Secondary Hyperparathyroidism (SHPT) and cachexia.

Disclosed are methods and systems for determining concentrations of a target molecule and a variant thereof in a sample. The sample can comprise or be suspected to comprise a target molecule and at least one variant thereof and is exposed to one or more recognition elements that bind to the target molecule and/or the at least one variant. A signal is detected that is associated with the binding of the target molecule and/or a signal is detected that is associated with the binding of the at least one variant to the one or more recognition elements. The concentration of the target molecule and/or the at least one variant thereof is determined based on the signals. The system can comprise a receiver adapted to receive a sample comprising or suspected to comprise a target molecule and the at least one variant thereof, the receiver comprising one or more recognition elements that bind to one or more epitopes in the target molecule and/or the at least one variant thereof.

A method for identifying a patient that is at risk for developing a thyroid disorder that occurs subsequent to treatment with a regimen that depletes lymphocytes, comprising determining whether antibodies directed against thyroid peroxidase or thyroid microsomes are present in the patient, wherein if the antibodies are present in the patient then the patient is at increased risk for developing a thyroid disorder. A particular embodiment is a method for identifying a patient with multiple sclerosis that is at risk for developing a thyroid disorder that occurs subsequent to treatment with a regimen that depletes CD52-positive cells, comprising determining whether antibodies directed against thyroid peroxidase or thyroid microsomes are present in the patient, wherein if the antibodies are present in the patient then the patient is at risk for developing the thyroid disorder.

A new method of in vitro monitoring and assessing the need of a medication which interferes with the regulation of the parathyroid hormone level in a kidney patient subject to oxidative stress, notably hemodialysis patients. FIG. 1 shows the distribution of n-oxPTH concentrations in 340 hemodialysis patients (224 men and 116 women) with a median age of 66 years (IQR, 56 to 75 years), a median time since initiation of dialysis (dialysis vintage) of 266 days (IQR, 31 to 1209 days), and a median dialysis dose (kt/V) of 1.2 (IQR, 1.1 to 1.3). The cause of chronic kidney disease was nephrosclerosis in 113 cases (33%), diabetic nephropathy in 107 cases (31%), chronic glomerular nephritis in 29 cases (9%), polycystic kidney disease in 9 cases (3%) and other/unknown in 82 cases (24%). The median n-oxPTH concentration was 5.9 ng/L (IQR, 2.4 to 14.0 ng/L). n-oxPTH concentrations were not different in men and women (5.9 ng/L; IQR, 2.4 to 14.2 ng/L; n=224; vs. 5.5 ng/L; IQR, 2.4 to 14.0 ng/L; n=116; p=0.915).

Disclosed are methods and systems for determining concentrations of a target molecule and a variant thereof in a sample. The sample can comprise or be suspected to comprise a target molecule and at least one variant thereof and is exposed to one or more recognition elements that bind to the target molecule and/or the at least one variant. A signal is detected that is associated with the binding of the target molecule and/or a signal is detected that is associated with the binding of the at least one variant to the one or more recognition elements. The concentration of the target molecule and/or the at least one variant thereof is determined based on the signals. The system can comprise a receiver adapted to receive a sample comprising or suspected to comprise a target molecule and the at least one variant thereof, the receiver comprising one or more recognition elements that bind to one or more epitopes in the target molecule and/or the at least one variant thereof.

It is an object to provide a culture method which is capable of maintaining and/or culturing iPS cell-derived intestinal stem cells, while maintaining the properties of intestinal stem cells. The induced pluripotent stem cell-derived intestinal stem cell-like cells are cultured in the presence of a GSK-3 inhibitor, a histone deacetylation inhibitor, and a serum replacement, or in the presence of a GSK-3 inhibitor and a serum replacement. Preferably, the culture is carried out under conditions in which one or more compounds selected from the group consisting of an epidermal growth factor, a TGF receptor inhibitor and a fibroblast growth factor are further present.

The present disclosure relates, in general, human antibodies against human parathyroid hormone receptor 1 (PTH1R) and methods of use of such antibodies in the treatment of cancer, Humoral Hypercalcemia of Malignancy (HHM), or Primary Hyperparathyroidism (PHPT) and Secondary Hyperparathyroidism (SHPT) and cachexia.

Provided are methods for detecting chromogranin A by mass spectrometry. In another aspect, provided herein are methods for quantitating chromogranin A by mass spectrometry. In another aspect, provided herein are methods for prognosis of or measuring the size of neuroendocrine tumors by mass spectrometry.

Methods for measuring and analyzing parathyroid hormone-related peptide (PTHrP) using LC-MS/MS, including applications of the methods thereof, are disclosed and discussed. Such methods can include, along with the use of an isotope-labeled internal standard, purifying PTHrP from a biological sample, proteolytically digesting the PTHrP, and measuring specific digestion products using the using LC-MS/MS.

A method for determining the amount of chromogranin A (CgA) in a sample includes: (a) purifying CgA in the sample; (b) adding an internal standard; (c) ionizing CgA and the internal standard to produce one or more CgA ion(s) and one or more internal standard ion(s) detectable by mass spectrometry; (d) determining the amount of the ion(s) from step (c) by mass spectrometry; and (e) correlating the amount of CgA in the sample to the amount of ion(s) measured in step (d).