Interaction between cytokines and ammonia in the mitochondrial permeability transition in cultured astrocytes.

Hepatic encephalopathy (HE) is the major neurological complication occurring in patients with acute and chronic liver failure. Elevated levels of blood and brain ammonia are characteristic of HE, and astrocytes are the primary target of ammonia toxicity. In addition to ammonia, recent studies suggest that inflammation and associated cytokines (CKs) also contribute to the pathogenesis of HE.

Marked potentiation of cell swelling by cytokines in ammonia-sensitized cultured astrocytes.

Background: Brain edema leading to high intracranial pressure is a lethal complication of acute liver failure (ALF), which is believed to be cytotoxic due to swelling of astrocytes. In addition to the traditional view that elevated levels of blood and brain ammonia are involved in the mechanism of brain edema in ALF, emerging evidence suggests that inflammatory cytokines also contribute to this process. We earlier reported that treatment of astrocyte cultures with a pathophysiological concentration of ammonia (5 mM NH4Cl) resulted in the activation of nuclear factor-kappaB (NF-κB) and that inhibition of such activation diminished astrocyte swelling, suggesting a key role of NF-κB in the mechanism of ammonia-induced astrocyte swelling.

Freeway safety as a function of traffic flow.

In this paper, we present evidence of strong relationships between traffic flow conditions and the likelihood of traffic accidents (crashes), by type of crash. Traffic flow variables are measured using standard monitoring devices such as single inductive loop detectors. The key traffic flow elements that affect safety are found to be mean volume and median speed, and temporal variations in volume and speed, where variations need to be distinguished by freeway lane.