The proliferation of mobile devices and the pervasiveness of wireless technology have provided a major impetus to replicate the network-based service discovery technologies in wireless and mobile networks. However, existing service discovery protocols and delivery mechanisms fall short of accommodating the complexities of the ad-hoc environment. They also place emphasis on device capabilities as services rather than device independent software services, making them unsuitable for m-commerce oriented scenarios. Konark is a service discovery and delivery protocol designed specifically for ad-hoc, peer-to-peer networks, and targeted towards device independent services in general and m-commerce oriented software services in particular. It has two major aspects -service discovery and service delivery. For discovery, Konark uses a completely distributed, peer-to-peer mechanism that provides each device the ability to advertise and discover services in the network. The approach towards service description is XML based. It includes a description template that allows services to be described in a human and software understandable forms. A micro-HTTP server present on each device handles service delivery, which is based on SOAP. Konark provides a framework for connecting isolated services offered by proximal pervasive devices over a wireless medium.

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The role of oxidative stress, neuro-inflammation and cholinergic dysfunction is already established in the development of Alzheimer’s disease (AD). Sinapic acid (SA), a hydroxylcinnamic acid derivative, has shown neuro-protective effects. The current study evaluates the neuro-protective potential of SA in intracerebroventricular streptozotocin (ICV-STZ) induced cognitive impairment in rats. Male Wistar rats were bilaterally injected with ICV-STZ. SA was administered intragastrically once daily for three weeks. Rats were divided into sham, ICV-STZ, STZ + SA (10 mg/kg), STZ + SA (20 mg/kg) and SA per se (20 mg/kg). Behavioral tests were assessed on day 0 and 21 days after STZ. Later, rats were sacrificed for biochemical parameters, pro-inflammatory cytokines, choline acetyltransferase (ChAT) expression and neuronal loss in the CA1 region of the hippocampus. The results showed that SA 20 mg/kg significantly (p < 0.05) improved cognitive impairment as assessed by Morris water maze and passive avoidance tests. SA 20 mg/kg reinstated the altered levels of GSH, MDA, TNF-α and IL-1β in the cortex and hippocampus. STZ-induced decreased expression of ChAT and neuronal loss were also significantly (p < 0.05) improved with SA. Our results showed that SA exhibits neuro-protection against ICV-STZ induced oxidative stress, neuro-inflammation, cholinergic dysfunction and neuronal loss, suggesting its potential in improving learning and memory in patients of AD.

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