NBC's GEnesis Broadcast Automation System: . . .

GEnesis is a system in use at the NBC television network for automating the composition and distribution of video. It works in a mission critical environment; a system failure could potentially result in a substantial loss of revenue for the network. Tcl/Tk has been an integral part of the operator interface and data handling portions of the GEnesis system from the earliest stages of prototyping. We originally planned to replace the system prototype based on Tcl/Tk with a production system built in a compiled, object-oriented language and using commercial component software. After the prototype phase was completed, the developers and management together decided to keep numerous system components in Tcl, while migrating some complex and performance-critical functions from Tcl to a C++ message passing architecture. This paper discusses that decision and presents our experience with converting the prototype into a fully functional system

Chronic immune activation and gut barrier dysfunction is associated with neuroinflammation in ART-suppressed SIV+ rhesus macaques.

HIV-associated neurocognitive disorders (HAND) affect ~40% of virally suppressed people with HIV (PWH), however, the precise viral dependent and independent changes to the brain are unclear. Here we characterized the CNS reservoir and immune environment of SIV-infected (SIV+) rhesus macaques during acute (n = 4), chronic (n = 12) or ART-suppressed SIV infection (n = 11). Multiplex immunofluorescence for markers of SIV infection (vRNA/vDNA) and immune activation was performed on frontal cortex and matched colon tissue. SIV+ animals contained detectable viral DNA+ cells that were not reduced in the frontal cortex or the gut by ART, supporting the presence of a stable viral reservoir in these compartments. SIV+ animals had impaired blood brain barrier (BBB) integrity and heightened levels of astrocytes or myeloid cells expressing antiviral, anti-inflammatory or oxidative stress markers which were not abrogated by ART. Neuroinflammation and BBB dysfunction correlated with measures of viremia and immune activation in the gut. Furthermore, SIV-uninfected animals with experimentally induced gut damage and colitis showed a similar immune activation profile in the frontal cortex to those of SIV-infected animals, supporting the role of chronic gut damage as an independent source of neuroinflammation. Together, these findings implicate gut-associated immune activation/damage as a significant contributor to neuroinflammation in ART-suppressed HIV/SIV infection which may drive HAND pathogenesis