Effect of intradialytic parenteral nutrition in patients with malnutrition-inflammation complex syndrome on body weight, inflammation, serum lipids and adipocytokines: results from a pilot study.

Objective: Evaluation of the influence of intradialytic parenteral nutrition (IDPN) in patients suffering from Malnutrition-Inflammation Complex Syndrome (MICS) on nutritional status, inflammation, adipocytokines and serum lipids.

Subjects: Six patients with MICS were assigned to IDPN, whereas six patients matched for age, sex, body mass index (BMI) and co-morbidity without malnutrition served as controls. Patients were recruited from Outpatient Dialysis Unit, Medical University Innsbruck and from Dialysis Unit, Hospital Feldkirch.

Secreted proNGF is a pathophysiological death-inducing ligand after adult CNS injury.

The unprocessed precursor of the neurotrophin nerve growth factor (NGF), proNGF, has been suggested to be a death-inducing ligand for the neurotrophin receptor p75. Whether proNGF is a true pathophysiological ligand that is secreted, binds p75, and activates cell death in vivo, however, has remained unknown. Here, we report that after brain injury, proNGF was induced and secreted in an active form capable of triggering apoptosis in culture.

Endogenous brain-derived neurotrophic factor and neurotrophin-3 antagonistically regulate survival of axotomized corticospinal neurons in vivo.

Neuronal growth factors regulate the survival of neurons by their survival and death-promoting activity on distinct populations of neurons. The neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) promote neuronal survival via tyrosine kinase (Trk) receptors, whereas NGF and BDNF can also induce apoptosis in developing neurons through p75(NTR) receptors in the absence of their respective Trk receptors. Using mutant mice and inactivation of neurotrophins and their receptors with antibodies in rats, we show that endogenous NT-3 induces death of adult BDNF-dependent, axotomized corticospinal neurons (CSNs).