Oxytocin/vasopressin-like peptides are important regulators of physiology and social behavior in vertebrates. However, the function of inotocin, the homologous peptide in arthropods, remains largely unknown. Here, we show that the level of expression of inotocin and inotocin receptor are correlated with task allocation in the antCamponotus fellah. Both genes are up-regulated when workers age and switch tasks from nursing to foraging. in situ hybridization revealed thatinotocin receptoris specifically expressed in oenocytes, which are specialized cells synthesizing cuticular hydrocarbons which function as desiccation barriers in insects and for social recognition in ants. dsRNA injection targetinginotocin receptor, together with pharmacological treatments using three identified antagonists blocking inotocin signaling, revealed that inotocin signaling regulates the expression ofcytochrome P450 4G1(CYP4G1) and the synthesis of cuticular hydrocarbons, which play an important role in desiccation resistance once workers initiate foraging.

The role that transforming growth factor-a (TGF-a) has in chronic pancreatitis and pancreatic cancer has not been fully elucidated. We evaluated the effects of TGF-a on the human pancreatic stellate cell (PSC) line RLT-PSC and primary human PSCs, and the expression levels of TGF-a and metalloproteinase-1 (MMP-1) in human chronic pancreatitis and pancreatic cancer tissues. TGF-a stimulated the proliferation and migration of PSCs. Although the mRNA expression levels of tissue inhibitor of metalloproteinase-1 and a1(I) collagen were unchanged, the mRNA expression levels of MMP-1 increased concomitant with increases in MMP-1 protein levels and collagenase activity. TGF-a-stimulated migration of RLT-PSC cells was partially blocked by tissue inhibitor of metalloproteinase-1 protein and MMP-1 small interfering RNA. MMP-1 was also observed to stimulate the migration of PSCs. TGF-a-induced MMP-1 expression was completely blocked by gefitinib in PSCs. The Ras-ERK and PI3/Akt pathways appear to be involved in the activation of MMP-1 in PSCs. Immunohistochemical analyses showed that MMP-1 expression was significantly increased in the pancreatic interstitial tissues in case of chronic pancreatitis or pancreatic cancer compared with those in case of normal pancreas. In conclusion, TGF-a increased proliferation and migration of PSCs. TGF-a-induced migration of cells may be partly due to upregulation of MMP-1. TGF-a and MMP-1 upregulation may contribute to the pathogenesis of chronic pancreatitis and pancreatic cancer.

A 66-year-old woman developed systemic sclerosis (SSc) after receiving interferon alphacon-1 (IFNalphacon-1; consensus interferon) therapy for chronic hepatitis C. She suffered from Raynauds phenomenon about 1 year after a course of IFNalphacon-1 therapy. The combination of proximal scleroderma, Raynauds phenomenon, and ANA positivity led to a diagnosis of systemic sclerosis (SSc). IFN has multiple effects on the immune system and is known to trigger the development of autoantibodies, as well as the onset or exacerbation of autoimmune disease. We suspect that the immunomodulatory effects of IFNalphacon-1 triggered the clinical manifestations of SSc in this patient. To our knowledge this is only the third case of SSc after IFNalpha therapy, and it is the first case associated with IFNalphacon-1 therapy.

IFN-based therapy following PSE had an advantage in the maintenance of higher platelet counts, and PSE possibly caused an increase in adherence to PEG-IFN. Although patients with genotype 2 might be better candidates for PSE, further evaluation is needed. Careful follow-up of PSE-treated patients, even though they may have achieved an SVR, is needed to detect HCC.

Elevated serum UA level was a notable AE associated with SOF/RBV therapy for CHG2. However, because of the small number of subjects, the exact frequency of AEs should be re-evaluated with larger cohorts. We need to remember that elevated serum UA level might develop during the therapy, especially at W1.