Based on evidence identifying cross-talk between pancreatic tumor cells and PaSC’s, our data suggest that bone marrow-derived PaSC’s may play an important, and supportive role in promoting carcinogenesis, the mechanisms of which remain to be elucidated. In addition, these models can potentially be used to selectively manipulate the genetic composition of PaSC’s, to facilitate the in vivo investigation of tumorhost interaction, where such models have not previously existed. About sixty percent of patients with septic shock develop adrenal insufficiency and subsequently may have higher risk of death. The mechanisms of impairement of the hypothalamopituitary-adrenal axis during critical illness are complex and poorly understood and may include decreased production of corticotropin-releasing hormone, adreno-corticotropic hormone and cortisol as well as dysfunction of their respective receptors. The antehypophyseal system includes the parvocellular neurons of the hypothalamic paraventricular nuclei producing CRH and vasopressin, and the antehypophysis where ACTH is synthesised. CRH neurons in the PVN project to median eminence, where CRH is released into the hypophyseal portal circulation to stimulate ACTH secretion via essentially CRH receptor 1, which is the most abundant form of CRH receptors. AVP produced by the parvocellular neurons also controls ACTH secretion via V1b receptor. Most human studies of HPA axis during sepsis have relied on circulating hormonal levels and have never included neuropathological studies. Previous experimental studies investigated hypothalamo-pituitary structures and showed that endotoxin or cytokines stimulate CRH neurons. However, they rarely assessed concomitantly the expression of AVP and CRH and their respective receptors as well as relationships between HPA activation and the severity of sepsis. In order to test the hypothesis that ACTH secretion is decreased secondarily to alteration of either CRH or AVP synthesis, we underwent a neuropathological study of the antehypophyseal system in patients who had died from septic shock and rats with experimental faecal peritonitis, which is considered one of the best model of human sepsis. Faecal peritonitis enables to obtain various degree of sepsis severity and seems an appropriate model for Paclitaxel assessing pathophysiological mechanisms of sepsisinduced hormonal disturbances. Fluid resuscitated rats were randomly divided as follows: 1) sham-operated controls that received no intraperitoneal injection but were otherwise treated identically; 2) Rats that underwent experimental peritonitis and were classified as severe sepsis if they did not die spontaneously and as septic shock if they died spontaneously rats). Sham and septic rats were killed by cervical dislocation at 24 or 48 hours after injection of slurry. All septic shock rats died within 36 hours. All septic and septic ED animals showed features of illness from about 12 h after injection of fecal slurry, including hunched posture, piloerection, and decreased movement and alertness. At 24 hours, there was a significant decrease in mean arterial pressure in septic rats.