Single-cell modeling of routine clinical blood tests reveals transient dynamics of human response to blood loss.

Low blood count is a fundamental disease state and is often an early sign of illnesses including infection, cancer, and malnutrition, but our understanding of the homeostatic response to blood loss is limited, in part by coarse interpretation of blood measurements. Many common clinical blood tests actually include thousands of single-cell measurements. We present an approach for modeling the unsteady-state population dynamics of the human response to controlled blood loss using these clinical measurements of single-red blood cell (RBC) volume and hemoglobin. We find that the response entails (1) increased production of new RBCs earlier than is currently detectable clinically and (2) a previously unrecognized decreased RBC turnover. Both component responses offset the loss of blood. The model provides a personalized dimensionless ratio that quantifies the balance between increased production and delayed clearance for each individual and may enable earlier detection of both blood loss and the response it elicits.

Detection and in vitro metabolism of the confiscated peptides BPC 157 and MGF R23H.

A new peptide, body protecting compound (BPC), BPC 157, and a variant of mechano-growth factor (MGF), MGF R23H, were identified in confiscated vials. BPC 157 has the amino acid sequence, GEPPPGKPADDAGLV, and is currently under investigation for the promotion of healing and recovery in a variety of tissues. In vitro metabolism experiments in plasma demonstrate that MGF R23H has good stability and should be detectable in urine, while BPC 157 forms a stable metabolite that should be detectable in urine. A weak cation exchange solid phase extraction method was validated for detection of BPC 157 in urine. The method has a limit of detection of 0.1 ng/mL, precision of less than 20%, and good linearity, r2 0.998. BPC 157 was stable in urine for at least 4 days. The specificity of the method is improved by measurement of a potential BPC metabolite along with the parent peptide. Copyright © 2016 John Wiley & Sons, Ltd.