The clinical application of impedance manometry is still being refined. This audit looked to examine whether impedance manometry had advantages over standard manometry in assessment of patients with dysphagia. Methods:  41 patients with the presenting symptom of dysphagia were assessed by combined MII and oesophageal manometry at a Wellington Hospital between February 2008 and December 2009. Each underwent manometry and MII selleck screening library using standardised techniques. Findings:  Achalasia was diagnosed in 23 patients (56.1%),

Ineffective oesophageal motility (IEM) in 5 patients (12.2%), Diffuse oesophageal Spasm (DES) in 7 patients (17.1%), and Nutcracker oesophagus in 2 patients (4.9%). 4 patients had normal manometry studies (9.8%). All patients with achalasia, IEM, and DES had abnormal bolus transit. All patients with normal manometry had abnormal bolus transit. Both patients with nutcracker oesophagus had normal bolus transit. 4 patients with achalasia had undergone previous Hellers myotomy. Two of these patients (50.0%) now had normal LES relaxation pressures, but all four still had abnormal oesophageal peristalsis and abnormal bolus transit.

Interpretation:  Multichannel Intraluminal Impedance manometry has advantages over standard manometry in characterising selleck products the physiological abnormalities associated with dysphagia. Patients in this study had severe defects including achalasia where bolus transit was invariably poor meaning little further information was gained. Extension of this study to include a wider group of patients with dysphagia may yield different results. “
“It is well established that interleukin (IL)-22 has hepatoprotective and antifibrotic functions in acute liver injury models; however, its function in patients with liver fibrosis and liver cirrhosis (LC) remains obscure. In the current study, we demonstrated that expression of numerous IL-22 pathway-associated

genes was significantly up-regulated in hepatitis B virus (HBV)-infected liver tissues, compared to normal controls, through microarray analysis. In MCE agreement with these findings, liver-infiltrating IL-22+ cells were largely increased in HBV-infected patients with LC, compared to those without LC or healthy subjects, and were positively associated with liver fibrosis staging scores. Immunohistochemistry and flow cytometric analyses revealed that IL-22 was produced by multiple intrahepatic immune cells and, preferentially, by T-helper (Th) 17 cells in LC patients. In an HBV transgenic (Tg) mouse model of T-cell-mediated chronic liver inflammation and fibrosis, blockade of IL-22 attenuated hepatic expression of chemokine (C-X-C motif) ligand 10 and chemokine (C-C motif) ligand 20 (CCL20) and subsequently reduced Th17 recruitment and liver inflammation and fibrosis progression. In vitro treatment with IL-22 stimulated hepatic stellate cells (HSCs) to secrete several chemokines and subsequently promoted Th17 cell chemotaxis.