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Responsiveness of male S. littoralis to the sex pheromone was investigated in the field in two experiments conducted in June and July, 2007. Traps baited with pheromone gland extracts were installed in a cotton field and the trap catch was collected every two hours during nighttime and every four hours during the daytime. The males exhibited an obvious diel rhythm I their attraction to the pheromone. Almost no males were trapped during daytime, considerable numbers of males were trapped during the first six hours of nighttime , and significantly larger numbers were trapped in the last four hours of nighttime. In addition to the experimental setting which controlled for many of the factors that may induce variation in trap catch, laboratory experiments were conducted to check if temporal change in eclosion rates could shape the pattern of trap catch. The diel emergence rhythm was found to be enough to account for the temporal variation in trap catch was due to inherent dial rhythm in male responsiveness to the sex pheromone, and that the rhythm may be controlled by internal clock mechanisms rather than exogenous factors. The significance of circadian behavioral response to sex pheromone in the life of S. littoralis and the practical implications of the results are discussed.

Background: The autoimmune disease type 1 diabetes mellitus (T1D) is associated with a defect in the immune response, which increases susceptibility to infection. We recently demonstrated that prolonged elevated levels of type 1 interferon (IFN) induce lymphocyte exhaustion during T1D. Aims: In the present study, we further investigated the effect of blocking the type I IFN receptor signaling pathway on diabetic dyslipidemia, in which an abnormal lipid profile leads to the exhaustion of B cells and alteration of their distribution and functions. Methods: T1D was induced in a mouse model by an intraperitoneal injection of a single dose (60 mg/kg) of streptozotocin (STZ). Three groups of mice were examined: a non-diabetic control group, a diabetic group and a diabetic group treated with an anti-IFN (alpha, beta and omega) receptor 1 (IFNAR1) blocking antibody to block type I IFN signaling. Results: We observed that induction of T1D was accompanied by a marked destruction of β cells and a reduction in the insulin levels in the diabetic group. Diabetic mice exhibited many changes, including alterations in their lipid profiles, expansion of splenic B cells, increased caspase-3, -8 and -9 activity, and apoptosis in peripheral B cells. Blocking type 1 IFN signaling in diabetic mice significantly returned the insulin and lipid profiles to normal levels, subsequently restored the B cell distribution, and rescued the peripheral B cells from apoptosis. Conclusion: Our data suggest the potential role of type I IFN in mediating diabetic dyslipidemia and an exhausted state of B cells during T1D.