Chronic cough (CC) is a common but poorly understood disease that has a negative impact on quality of life. For years, clinicians have been trying to find the underlying diagnosis and using existing disease models to describe the patients\' illness. This presents a confusing picture of CC. Most patients with CC present with hypersensitivity of the cough reflex, which is characterised by laryngeal paraesthesia and an increased response to the tussive stimuli or an innocuous stimulus that would not trigger coughing in healthy people. Recently, it has been proposed that CC is a unique disease characterised by vagal hypersensitivity that projects to the central nervous system altering responsiveness. The evidence supports the hypothesis that CC is primarily a neurological disorder, consisting of different phenotypes.

Preparing the patient for home parenteral nutrition (HPN) is a collaborative effort among many different clinicians. Identifying patients who will transition home with parenteral nutrition (PN) as early as possible allows for a thoughtful and safe approach. Communication regarding the HPN goals is critical to the patient\'s success, whether the requirement for PN is temporary or permanent. Management of these complex patients is best served by a multidisciplinary team with expertise in the area of nutrition support. Adherence to available guidelines that define best practice is imperative in all aspects of care for the patient on HPN.

BACKGROUND: Intestinal inflammation is well known to cause gut dysmotility through the effects on the enteric nervous system. Glial-derived neurotrophic factor (GDNF) has been demonstrated to have anti-inflammatory effects and neuronal protective actions. The aim of this study was to investigate whether the GDNF could improve inflammation-induced gut dysmotility.
METHODS: Recombinant adenoviral vectors encoding GDNF (Ad-GDNF) were administered intracolonically in experimental colitis induced by dextran sulfate sodium (DSS). The disease activity index (DAI) and histological score were measured. Colonic transit was measured by using phenol red and assessed with the geometric center. PGP 9.5 immunostaining was used to examine the number and distribution of enteric neurons. The expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and myeloperoxidase (MPO) activity were measured by ELISA assay. The expression of Akt, caspase-3, bcl-2 and PGP 9.5 was analyzed by western blot assay.
RESULTS: A significant neuronal cell loss and a significant delay in colonic transit accompanied with the neuronal loss following inflammation were observed. GDNF prevented partially the loss of enteric neurons and ameliorated significantly experimental colitis and delayed colonic transit by, at least in part, down-regulation of TNF-α and IL-1β expression, decrease of infiltration of leukocytes, and inhibition of neuronal cell apoptosis.
CONCLUSIONS: GDNF reduces inflammation and improves delayed colonic transit in DSS-induced colitis. GDNF may be a useful therapeutic agent for the treatment of gut dysmotility in patients with UC.