A method for therapy monitoring, comprising: the prognosis, risk assessment and/or risk stratification of a subsequent adverse event in the health of a patient; providing a sample of said patient, wherein the patient was diagnosed as critically ill and medical treatment initiated, wherein the sample is isolated from the patient after diagnosis and treatment initiation; determining a level of proADM or fragment(s) thereof in said sample, wherein said level of proADM or fragment(s) thereof correlates with the likelihood of a subsequent adverse event in the health of said patient. In a preferred embodiment the invention relates to a method comprising additionally determining a level of procalcitonin (PCT) or fragment(s) thereof in a sample isolated from the patient. Optionally, further determining a level of PCT or fragment(s) thereof in samples isolated from the patient and using the PCT levels also in the prognosis, risk assessment and/or risk stratification.

A whole blood filtration device is provided with a filter membrane separating a feeding volume and a clean side of the filter membrane from each other. The feeding volume communicates with a first feeding side opening and with a second feeding side opening. The filter membrane has pores with a pore size that ensures permeability of the filter membrane to blood plasma/serum and that retains blood cells. The first feeding side opening can be coupled to a first blood pump for feeding blood from the first feeding side opening into the feeding volume so that blood plasma/serum permeates the filter membrane and blood cells, retained by the filter membrane, exit from the feeding volume through the second feeding side opening.

The present invention relates to the field of treating iron deficiency with IV iron carbohydrate complexes such ferric carboxymaltose, monitoring or identifying subjects to determine their eligibility for being administered said IV iron carbohydrate complexes, and combining said IV iron carbohydrate complexes with additional drugs in order to mitigate or reduce side effects induced by said IV iron carbohydrate complexes.

The present invention relates to a rapid assay for detection of human cellular fibronectin (c-Fn) where ELISA-based assays have previously been developed for detecting and measuring cellular fibronectin in biological fluids, but these methods are too time-consuming for practical clinical diagnostic use. The assay of the present invention enables prediction of bleeding events on a rapid timescale. Described as well are high affinity human monoclonal antibodies, particularly those directed against isotopic determinants of cellular fibronectin (c-Fn), as well as direct equivalents and derivatives of these antibodies. These antibodies bind to their respective target with an affinity at least 100 fold greater than they do to plasma fibronectin, and enable assays to be created that detect c-Fn in less than 30 minutes in a variety of detection formats, and in some detection formats less than 15 minutes. These antibodies are useful for diagnostics, particularly prediction of bleeding events, prophylaxis and treatment of disease.

A method and device for analyzing a hematologic sample centrifuged within a capillary tube is provided. The device includes a tube holder, a sample imaging device, a processor, and a sample data display. The sample imaging device is operable to create a digital image of the sample within a region of the tube. The region is defined by substantially all of the radial width and axial length of the sample residing within the internal cavity of the tube in the region where the float resides after centrifugation. The sample imaging device is operable to produce signals representative of the image. The processor is adapted to produce information relating to bands of interest within the image based on the signals from the sample imaging device. The sample data display is adapted to display the results therefrom and/or a digital image of the sample within the region.

The invention relates to a method of therapy guidance, stratification and/or monitoring of fluid therapy based on proadrenomedullin (proADM) levels. The invention therefore relates to a method for therapy guidance, stratification and/or monitoring of a fluid therapy, comprising providing a sample of said patient, determining a level of pro adrenomedullin (proADM) or fragment(s) thereof in said sample, wherein said level of proADM or fragment(s) thereof indicates the prescription of fluid therapy to be administered to the patient. The invention further relates to methods for guiding fluid therapy volume and to methods of treating disease using fluid therapy based on the proADM stratification of patients based on the methods described herein.

The disclosure relates to identifying novel therapeutic targets and/or diagnostic and/or prognostic markers by correcting abnormal RhoH expression in a hematopoietic cell.

Disclosed herein are antibodies specific for erythroferrone and assays comprising the antibodies. Also disclosed are methods for using the assays for the diagnosis or monitoring of disease.

A whole blood filtration device is provided with a filter membrane separating a feeding volume and a clean side of the filter membrane from each other. The feeding volume communicates with a first feeding side opening and with a second feeding side opening. The filter membrane has pores with a pore size that ensures permeability of the filter membrane to blood plasma/serum and that retains blood cells. The first feeding side opening can be coupled to a first blood pump for feeding blood from the first feeding side opening into the feeding volume so that blood plasma/serum permeates the filter membrane and blood cells, retained by the filter membrane, exit from the feeding volume through the second feeding side opening.

A COTL1 gene or protein maintains and regulates the homeostasis of hematopoietic stem cells. A method of diagnosis and treatment of blood-related disease caused either by abnormalities in the homeostasis of hematopoietic stem cells, which result from a mutation in the COTL1 gene or a decrease in the expression of the COTL1 protein, or by an imbalance between the differentiation or proliferation and damage or death of hematopoietic stem cells, or by abnormalities in mitochondrial homeostasis. The COTL1 gene or protein plays an important role in regulating mitochondrial morphology, and when it is knocked down, the number of hematopoietic stem cells decreases.