Cooperation across multiple healthcare clinics on the cloud

Many healthcare units are creating cloud strategies and mi- gration plans in order to exploit the benefits of cloud based computing. This generally involves collaboration between healthcare specialists and data management researchers to create a new wave of healthcare tech- nology and services. However, in many cases the technology pioneers are ahead of government policies as cloud based storage of healthcare data is not yet permissible in many jurisdictions. One approach is to store anonymised data on the cloud and maintain all identifying data locally. At login time, a simple protocol can be developed to allow clinicians to combine both sets of data for selected patients for the current session. However, the management of o↵-cloud identifying data requires a frame- work to ensure sharing and availability of data within clinics and the ability to share data between users in remote clinics. In this paper, we introduce the PACE healthcare architecture which uses a combination of Cloud and Peer-to-Peer technologies to model healthcare units or clin- ics where o↵-cloud data is accessible to all, and where exchange of data between remote healthcare units is also facilitated

Inhibition of 26S Protease Regulatory Subunit 7 (MSS1) Suppresses Neuroinflammation

Recently, researchers have focused on immunosuppression induced by rifampicin. Our previous investigation found that rifampicin was neuroprotective by inhibiting the production of pro-inflammatory mediators, thereby suppressing microglial activation. In this study, using 2-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS), we discovered that 26S protease regulatory subunit 7 (MSS1) was decreased in rifampicin-treated microglia. Western blot analysis verified the downregulation of MSS1 expression by rifampicin. As it is indicated that the modulation of the ubiquitin-26S proteasome system (UPS) with proteasome inhibitors is efficacious for the treatment of neuro-inflammatory disorders, we next hypothesized that silencing MSS1 gene expression might inhibit microglial inflammation. Using RNA interference (RNAi), we showed significant reduction of IkBα degradation and NF-kB activation. The production of lipopolysaccharides-induced pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), nitric oxide, cyclooxygenase-2, and prostaglandin E2 were also reduced by MSS1 gene knockdown. Taken together, our findings suggested that rifampicin inhibited microglial inflammation by suppressing MSS1 protein production. Silencing MSS1 gene expression decreased neuroinflammation. We concluded that MSS1 inhibition, in addition to anti-inflammatory rifampicin, might represent a novel mechanism for the treatment of neuroinflammatory disorders

Effect of rifampin on the immune response in mice.

In an investigation of the effect of rifampin on the immune response in mice, the cellular immunity was evaluated with the split-heart allograft technique. The survival time of the heart in animals treated with rifampin at a dose of 20 mg/kg per day from the day of the transplantation until the graft was rejected was longer (33.7 days, P less than 0.001) than that of animals not treated with antibiotics (14.5 days). When rifampin was given at a dose of 5 mg/kg per day for the same period, the mean survival time of allografts was 19.5 days. The number of demonstrable plaques of hemolysis and the humoral antibodies to sheep erythrocytes were also reduced by a human therapeutic dose (20 mg/kg per day). However, the suppression of the humoral immune response was probably of more limited biological significane, suggesting a differential sensitivity to rifampin. In contrast to rifampin, benzylpenicillin had no noteworthy inhibiting effect on the cellular or humoral immune response