Hence, a noxious our site stimulation pressure of 80 mmHg was used (4, 31, 39, 42). In humans, subjective assessment of the evoked sensation made it possible to obtain the ��true�� sensation and individualize the stimulus intensity corresponding to pain detection threshold. However, one difficulty with using this stimulation level is that rectal mechanical distension does not always produce a painful sensation and instead induces a strong urge to defecate before pain levels can be reached (15, 16). This was consistent with findings in the present study, as five subjects did not reach pain detection threshold at the maximum inflation volume. In this study, a sufficient synchronization between pump on
Intrahepatic bile ducts constitute a complex 3-dimensional tubular network, the biliary tract, through which bile is transported to the duodenum.

Human bile is sterile under normal physiological conditions (1); however, the biliary tract is periodically exposed to pathogens, including Escherichia coli and the protozoan parasite Cryptosporidium parvum, or pathogen-derived molecules, including Gram-negative bacteria-derived lipopolysaccharide (LPS).2 Upon pathogen recognition, a phenotypic transition occurs through which biliary epithelial cells (cholangiocytes) promote the innate and adaptive immune responses (1,�C4). Indeed, cholangiocytes express a variety of pathogen recognition receptors and actively participate in the innate immune response through the secretion of cytokines/chemokines (5, 6), expression of adhesion molecules (7,�C9), and antimicrobial peptides (1, 10).

Expression of these immune-associated genes is a highly regulated process to assure that the epithelium recognizes and responds to invading pathogens, but does not induce injury through an inappropriate immune response. Recent reports suggest the microRNA machinery contributes to the regulation of the immune-associated gene expression. MicroRNAs are small (21�C23 nt) RNA molecules that target and regulate the stability or translational efficiency of mRNAs (11). These regulatory RNAs are transcribed as mono- or polycistronic primary microRNAs (pri-microRNAs), which are sequentially processed to precursor and the functionally active mature microRNA. The molecular mechanisms regulating the expression of most microRNAs remain largely unknown.

Using a human Brefeldin_A cholangiocyte cell culture model of biliary cryptosporidiosis, we previously reported that let-7i, a member of the let-7 family of microRNAs, targets Toll-like receptor 4 mRNA and limits the expression of this pathogen molecular pattern receptor resulting in decreased primary and mature let-7i expression (3). These results suggested that the expression of let-7i is responsive to pathogen recognition and regulated through primary-microRNA transcription.