SUMMARY The results of a combined clinical and laboratory study in 55 patients throughout the leprosy spectrum are reported. Thirty one of these patients suffered from an inflammatory peripheral polyarthritis which has not been previously described and which was unassociated with the characteristics of erythema nodosum leprosum reactions or with Charcot's joints. a2 Macroglobulin was raised significantly only in those patients with leprosy and arthritis.
Instituting a field-based CURE for all biology and allied majors creates a transformative experience wherein students view themselves as active members in the scientific community who are connected to the place they live, increasing equity that can have far-reaching implications.
The paralysis tick Ixodes holocyclus bites humans, companion animals, and livestock in eastern Australia leading to symptoms that range between negligible and severe. Bandicoots (Family Peramelidae) are commonly cited as the "primary host" of I. holocyclus in the media and blamed for outbreaks of ticks and disease fears, creating conflicts between conservation and tick management. We discuss how evidence for bandicoots being essential to the I. holocyclus life cycle has originated from a small number of papers that were limited in scope. False assumptions of host-specificity have contributed to the extrapolation of studies in one ecosystem, yet no study has sampled the full range of hosts of I. holocyclus to understand the relative role of each species across the entire range of I. holocyclus in relation to health threats. Bandicoots are one of many potential tick hosts but cannot yet be considered the "primary host" of I. holocyclus. Researchers and media should refrain from highlighting bandicoots as the main I. holocyclus host without mentioning caveats, and work towards gaining a better understanding of tick-host interactions across the range of I holocyclus in order to better understand and mitigate public health risks.
Poor nutrition plays a fundamental role in the development of insulin resistance, an underlying characteristic of type 2 diabetes. We have previously shown that high-fat diet-induced insulin resistance in rats can be ameliorated by a single glucose meal, but the mechanisms for this observation remain unresolved. To determine if this phenomenon is mediated by gut or hepatoportal factors, male Wistar rats were fed a high-fat diet for 3 weeks before receiving one of five interventions: high-fat meal, glucose gavage, high-glucose meal, systemic glucose infusion or portal glucose infusion. Insulin sensitivity was assessed the following day in conscious animals by a hyperinsulinaemic-euglycaemic clamp. An oral glucose load consistently improved insulin sensitivity in high-fat-fed rats, establishing the reproducibility of this model. A systemic infusion of a glucose load did not affect insulin sensitivity, indicating that the physiological response to oral glucose was not due solely to increased glucose turnover or withdrawal of dietary lipid. A portal infusion of glucose produced the largest improvement in insulin sensitivity, implicating a role for the hepatoportal region rather than the gastrointestinal tract in mediating the effect of glucose to improve lipid-induced insulin resistance. These results further deepen our understanding of the mechanism of glucose-mediated regulation of insulin sensitivity and provide new insight into the role of nutrition in whole body metabolism.
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