Objective. To document the histology of Ross River virus (RRV) arthritis and to examine inflamed synovium for viral RNA. Methods. Biopsy tissue from the inflamed knees of 12 patients with RRV infection was studied using conventional and immunostaining techniques. Reverse transcriptase-polymerase chain reaction technology was used to probe for the presence of viral RNA in the synovial biopsy samples and in serum. Results. Hyperplasia of the synovial lining layer, vascular proliferation, and mononuclear cell infiltration were the main histologic changes. RRV RNA was found in knee biopsy tissue that was obtained from 2 patients at 5 weeks after the onset of symptoms. Conclusion. RRV RNA was identified in inflamed synovium more than a month after symptoms began. Inflammation was apparent in the absence of detectable virus in the majority of patients.

There is a lack of information pertaining to the effects of transport stress on the acid-base physiology of ruminants. The effect of transportation and/or feed and water deprivation on acid-base balance was studied using 19 2-yr-old Bos indicus steers. The steers were allocated to one of three groups: 1) control, offered ad libitum access to feed and water (n = 8); 2) water and feed deprived, offered no feed or water for 60 h (n = 6); and 3) transported, offered no feed or water for 12 h, and then transported for 48 h (n = 5). Blood gases, electrolytes, lactate, total protein, albumin, anion gap, strong ion difference, and total weak acids were determined at the conclusion of transportation. Arterial blood pH did not differ among the experimental groups. Partial pressure of carbon dioxide (pCO2) was lower for the water and feed deprived (P = 0.023) group than for the control group. Plasma total protein, albumin and total weak acid concentrations were higher for the transported (P = 0.001, P = 0.03, P = 0.01) and water- and feed-deprived (P = 0.000, P = 0.003, P = 0.001) groups, respectively, compared with the control group. Transported animals had a lower plasma concentration of potassium (P = 0.026) compared with the control animals. This study demonstrates that although blood pH remains within normal values in transported and fasted steers, the primary challenge to a transported or feed- and water-deprived animal is a mild metabolic acidosis induced by elevated plasma proteins, which may be the result of a loss of body water. The loss of electrolytes had little effect on the acid-base balance of the animals.

The effect on water and electrolyte balance of stress, simulated by intravenous infusion of cortisol, was studied using 24 18-mo-old Merino wethers (37.0 +/- 0.94 kg mean body weight [BW]) over 72 h. The sheep were allocated to one of four groups: 1) no water/no cortisol (n = 6); 2) water/no cortisol (n = 4); 3) no water/cortisol (n = 6); and 4) water/cortisol (n = 4). Animals allocated to the two cortisol groups were given 0.1 mg x kg BW(-1) x h(-1) of hydrocortisone suspended in isotonic saline to simulate stress for the duration of the experiment. Total body water, plasma cortisol, osmolality and electrolytes, and urine electrolytes were determined at 24-h intervals for 72 h. In the presence of cortisol, total body water was maintained in the face of a water deprivation insult for 72 h. Water deprivation alone did not induce elevated plasma concentrations of cortisol, in spite of a 13% loss of total body water between 48 and 72 h. Infusion of cortisol was found to increase urine output (P = 0.003) and decrease total urinary sodium output (P = 0.032), but had no effect on plasma electrolyte levels or water intake. Water deprivation was found to increase plasma sodium concentrations (P = 0.037). These results indicate that sheep given cortisol to simulate stress suffer from a loss of body water in excess of that associated with a loss of electrolytes, and support the hypothesis that elevated physiological concentrations of cortisol induce a diuresis in ruminants that contributes to dehydration.

Traumatic brain injury results in an increased brain energy demand that is associated with profound changes in brain glycolysis and energy metabolism. Increased glycolysis must be met by increasing glucose supply that, in brain, is primarily mediated by two members of the facilitative glucose transporter family, Glut1 and Glut3. Glut1 is expressed in endothelial cells of the blood-brain barrier (BBB) and also in glia, while Glut3 is the primary glucose transporter expressed in neurons. However, few studies have investigated the changes in glucose transporter expression following traumatic brain injury, and in particular, the neuronal and glial glucose transporter responses to injury. This study has therefore focussed on investigating the expression of the glial specific 45-kDa isoform of Glut1 and neuronal specific Glut3 following severe diffuse traumatic brain injury in rats. Following impact-acceleration injury, Glut3 expression was found to increase by at least 300% as early as 4 h after induction of injury and remained elevated for at least 48 h postinjury. The increase in Glut3 expression was clearly evident in both the cerebral cortex and cerebellum. In contrast, expression of the glial specific 45-kDa isoform of Glut1 did not significantly change in either the cerebral cortex or cerebellum following traumatic injury. We conclude that increased glucose uptake after traumatic brain injury is primarily accounted for by increased neuronal Glut 3 glucose transporter expression and that this increased expression after trauma is part of a neuronal stress response that may be involved in increasing neuronal glycolysis and associated energy metabolism to fuel repair processes.