Reduced fitness among resistant versus susceptible individuals slows resistance evolution and makes it easier to manage. A loss of resistance costs could indicate novel adaptations or mutations contributing to resistance. We measured costs of resistance to imidacloprid in a Massachusetts resistant population compared with a Massachusetts susceptible population in 1999 in terms of fecundity, hatching success, egg development time, and sprint speed. Resistance was additive and seemed to be polygenic with high heritability. The fecundity cost appeared overdominant in 1999, and the hatch rate cost was partly recessive in 1999, but neither was significantly different from dominant or recessive. In 2004, we repeated our measures of resistance costs in Massachusetts in terms of fecundity and hatching success, and we added a new resistant population from Maine. In 2005, we compared development time of Maine resistant and the laboratory susceptible colony eggs. Significant fecundity costs of resistance were found in both population in both 1999 and 2004, and significant egg developmental time costs were found in 1999 and 2005. However, the hatching success costs of resistance were significant in 1999 and not apparent in 2004, suggesting some modification or replacement of the resistance genes in the intervening time.

Reduced fitness among resistant versus susceptible individuals slows resistance evolution and makes it easier to manage. A loss of resistance costs could indicate novel adaptations or mutations contributing to resistance. We measured costs of resistance to imidacloprid in a Massachusetts resistant population compared with a Massachusetts susceptible population in 1999 in terms of fecundity, hatching success, egg development time, and sprint speed. Resistance was additive and seemed to be polygenic with high heritability. The fecundity cost appeared overdominant in 1999, and the hatch rate cost was partly recessive in 1999, but neither was significantly different from dominant or recessive. In 2004, we repeated our measures of resistance costs in Massachusetts in terms of fecundity and hatching success, and we added a new resistant population from Maine. In 2005, we compared development time of Maine resistant and the laboratory susceptible colony eggs. Significant fecundity costs of resistance were found in both population in both 1999 and 2004, and significant egg developmental time costs were found in 1999 and 2005. However, the hatching success costs of resistance were significant in 1999 and not apparent in 2004, suggesting some modification or replacement of the resistance genes in the intervening time.

Mixed corticomedullary adrenal tumours (MCMT) are rare. We describe the second reported case of a male patient presenting with hypertension and Cushing syndrome with MCMT. A man aged 48 years presented with hypertension and signs of Cushing syndrome. 24-hour urine cortisol was elevated, with detectable adrenocorticotropic hormone (ACTH). A high-dose dexamethasone suppression test indicated an adrenal or ectopic Cushing syndrome. Plasma metanephrines were normal. A 3 cm left adrenal mass was identified without potential ectopic sources of ACTH on imaging. After induction of anaesthesia for laparoscopic adrenalectomy, the patient developed resistant hypertension with stress-dose hydrocortisone administration. Surgery was cancelled and repeat testing revealed elevated plasma metanephrines. α-Blockade was administered for a presumed coexisting pheochromocytoma, and the patient underwent adrenalectomy. Pathology revealed an MCMT. This case highlights the importance of a thorough biochemical evaluation in patients with adrenal masses to rule out multiple hormone producing tumours.