Security is a critical and vital task in wireless sensor networks (WSNs), therefore different key management systems have been proposed, many of which are based on symmetric primitives. Such systems are very energy efficient, but they lack some other desirable characteristics. On the other hand, systems based on public key cryptography (PKC) have those desirable characteristics, but they consume more energy. Recently based on authenticated messages from base station (BS) a new PKC– based key agreement protocol was proposed. We show this method is susceptible to a form of denial of service (DOS) attack where resources of network can be exhausted with bogus messages. Then, we propose two different improvements to solve this vulnerability. Simulation results show that these new protocols retain desirable characteristics of the basic method but solve its deficiencies.

Diabetes is a prevalent disease in our country as it is worldwide. The rat is a suitable animal model for these studies. Protein kinase C is an enzyme which in its inactive form is located in the cytoplasm, but when activated (with calcium and phospholipid), translocate to the plasma membrane and phosphorylate the target proteins. Effects of this protein kinase and its isoenzymes in diabetic complications has been implicated. In this study, diabetes was induced with streptozotocin in the rat, and the effect of nifedipine (a calcium channel blocker), and polymyxin B sulphate (protein kinase C inhibitor) was investigated. The results showed that the levels ofthe, urea (two-fold), creatinine (60%), triglyceride (two-fold) and liver enzymes (two-fold) were significantly increase in the diabetic group. While in the other diabetic group, which was treated with oral nifedipine, although urea and creatinine levels were increased, had no increased in enzyme levels significantly different from those of the control group. The diabetic group treated with polymyxin had metabolites and enzyme levels equal to the control group except glucose level which was increased and liver glycogen storage which was decreased significantly. Protein kinase C activity in the cytoplasm of untreated diabetic group liver was increased comparing to its control group (573 ± 56 vs 400 ± 62). The enzyme activity in the plasma membranes of untreated and nifedipine treated diabetic groups was significantly increased, but in the polymyxin treated diabetic group the enzyme activity was close to the control group. Enzyme activity in the kidney cell membranes was significantly increased only in the untreated diabetic group. These results show that polymyxin is more effective than nifedipine against protein kinase C activity in diabetic complications. In conclusion, the results of this and other studies show that protein kinase C contributes to diabetic complications. We hope that future drug designers will target protein kinase C isozymes with specific inhibitors.

Objective(s): The present research aimed to identify the functional effects and underlying mechanisms of metformin on the rat thoracic aorta. Materials and Methods: Thoracic aorta segments of Wistar Albino rats were put in the chambers of an isolated tissue bath system. The resting tone was adjusted to 1 g. Following the equilibration time, potassium chloride or phenylephrine was used to contract the vascular segments. The vessel segments were cumulatively treated with metformin (10-7 –, 10-3 M) when a steady contraction was achieved. The described experimental approach was repeated after incubations with signaling pathway inhibitors and selective blockers of potassium channels to identify the effect mechanisms of metformin. Results: Metformin had a potent vasorelaxant effect in a concentration-dependent way (P<0. 001). After the endothelium was removed, the vasorelaxant effect level of metformin was significantly reduced. The level of vasorelaxant effect of metformin was increased by the maintenance of perivascular adipose tissue. Following administrations of L-NAME, methylene blue, compound C, BIM-I, and potassium channel blockers, the level of vasodilatory action of metformin was significantly reduced (P<0. 001). Conclusion: According to the results of this investigation, metformin significantly relaxes the thoracic aorta segments of rats. Metformin-mediated vasorelaxation involves the activation of numerous subtypes of potassium channels, including BKCa, IKCa, Kv, Kir, and K2p channels, as well as endothelium-dependent processes, including AMPK and eNOS/NO/sGS signaling pathways. Moreover, metformin-induced vasorelaxation is mediated through PVAT activation and the PKC signaling pathway.

Background and aims: Studies have recently shown that intermittent normobaric hyperoxia has a significant therapeutic effect on the treatment of acute ischemia, this effect so-called preconditioning. In this study intermittent normobaric effect of hyperoxia and PKC activity in the BBB permeability and behavioral assessment were evaluated.Methods: In this experimental study 36 wistar rat were divided to 6 groups as follow: normoxi (shem), normoxi + CHEL, normoxi + halt, normoxi + halt + CHEL, hyproxi + halt, hyperoxi + halt + CHEL, (n=6) in each group. Chelerythrin chlorid (CHEL) was used as a systemically inhibitor of PKC.24 hours later, rats were subjected to 60 min of right middle cerebral artery occlusion (MCAO). The hyperoxia and normoxia groups were exposed to 95% and 21% respectively, for 4 h/day, 6 continuous days. After 24 h reperfusion, neurological deficit scores and BBB permeability was assessed. Data were analyzed using two way ANOVA and Bonferroni test.Results: Preconditioning with intermittent normobaric hyperoxia decreased neurologic deficit scores and BBB permeability. Inhibition of PKC resulted in the increase of neurologic deficit scores; which improved with hyperoxia (P<0.001). PKC inhibition, independent of hyperoxia improved the BBB function (P<0.001).Conclusion: With the deployment of hyperoxia and specific subunits of PKC during the stroke, stability of BBB integrity and improvement of neurological deficit scores occur.

Background: The aim of this study was to investigate the possible role of Protein Kinase Cᵧ (PKCᵧ ) in morphine tolerance and induced hyperalgesia following repeated morphine administration in male rats. Material and Methods: Rats were divided into 4 groups for testing. The groups consisted of control (saline), morphine tolerance and hyperalgesia, metformine, morphine tolerance and hyperalgesia + metformine. First morphine (10mg/kg, s. c) administrated daily up to 14 days subcutaneously. Hargreaves' behavioral test was done before (control) and after the first dose of morphine on first day and then on day14th after last injection to evaluate morphine tolerance. To consider morphine hyperalgesia PWL was assessed by Hargreaves test before and after first morphine injection on first day and then on day 14th before last injection of morphine and on day16th two days after last injection of morphine. The expression of spinal PKCᵧ measured on day 14th and 16th. Metformin 100mg/kg, co-administrated with morphine daily up to 14 days then PWL and PKCᵧ expression were assessed as mentioned above. Results: The results showed significant tolerance and hyperalgesia on day 14th and 16th in compare to control. PKCᵧ expression also increased significantly on day 14th and 16th in compare to control but there was no significant differences in compare of day 14th and 16th. Co-administration of metformin and morphine up to 14 days increased PWL in morphine tolerance and reduced hyperalgesia and PKCᵧ expression. Conclusion: Results showed that increasing of spinal PKCᵧ expression in chronic morphine administration may involve in morphine tolerance and hyperalgesia.