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The Genetic Sexing Strain (GSS) of Anastrepha ludens (Loew) Tapachula-7 (Tap-7) produces males emerged from brown pupa [used for the Sterile Insect Technique (SIT)] and females from black pupa (a by-product) that can be sorted by a mechanical process. The early sorting provides young black pupae which were assessed as host of the parasitoid Coptera haywardi (Oglobin). This required an assessment of possible deleterious effects to A. ludens males (that emerged from the brown pupae). Our results demonstrate the host viability of the young Tap-7 black pupae. Nevertheless, A. ludens males obtained from brown pupae showed significantly reduced emergence (77.28%) and flight ability (63.33%). This negatively affected the emission of male signals for mating and, therefore, the competitiveness of A. ludens GSS used for the SIT. Our results suggest that there is no immediate alternative to the use of Tap-7 young black pupae as hosts for the mass rearing of C. haywardi. [ABSTRACT FROM AUTHOR]

Purpose: Over 300,000 ventral hernia repairs (VHRs) are performed each year in the US. We sought to assess the economic burden related to ventral hernia recurrences with a focused comparison of those with the initial open versus laparoscopic surgery.Methods: The Premier Alliance database from 2009 to 2014 was utilized to obtain patient demographics and comorbid indices, including the Charlson comorbidity index (CCI). Total hospital cost and resource expenses during index laparoscopic and open VHRs and subsequent recurrent repairs were also obtained. The sample was separated into laparoscopic and open repair groups from the initial operation. Adjusted and propensity score matched cost outcome data were then compared amongst groups.Results: One thousand and seventy-seven patients were used for the analysis with a recurrence rate of 3.78 %. For the combined sample, costs were significantly higher during recurrent hernia repair hospitalization ($21,726 versus $19,484, p < 0.0001). However, for index laparoscopic repairs, both the adjusted total hospital cost and department level costs were similar during the index and the recurrent visit. The costs and resource utilization did not go up due to recurrence, even though these patients had greater severity during the recurrent visit (CCI score 0.92 versus 1.06; p = 0.0092). Using a matched sample, the total hospital recurrence cost was higher for the initial open group compared to laparoscopic group ($14,520 versus $12,649; p = 0.0454).Conclusions: Based on our analysis, need for recurrent VHR adds substantially to total hospital costs and resource utilization. Following initial laparoscopic repair, however, the total cost of recurrent repair is not significantly increased, as it is following initial open repair. When comparing the initial laparoscopic repair versus open, the cost of recurrence was higher for the prior open repair group. [ABSTRACT FROM AUTHOR]

Cerebral ischemia and excitotoxic injury induce transient or permanent bioenergetic failure, and may result in neuronal apoptosis or necrosis. We have previously shown that ATP depletion and activation of AMP-activated protein kinase (AMPK) during excitotoxic injury induces neuronal apoptosis by transcription of the pro-apoptotic BH3-only protein, Bim. AMPK, however, also exerts pro-survival functions in neurons. The molecular switches that determine these differential outcomes are not well understood. Using an approach combining biochemistry, single-cell imaging and computational modeling, we here demonstrate that excitotoxic injury activated the bim promoter in a FOXO3-dependent manner. The activation of AMPK reduced AKT activation, and led to dephosphorylation and nuclear translocation of FOXO3. Subsequent mutation studies indicated that bim gene activation during excitotoxic injury required direct FOXO3 phosphorylation by AMPK in the nucleus as a second activation step. Inhibition of this phosphorylation prevented Bim expression and protected neurons against excitotoxic and oxygen/glucose deprivation-induced injury. Systems analysis and computational modeling revealed that these two activation steps defined a coherent feed-forward loop; a network motif capable of filtering any effects of short-term AMPK activation on bim gene induction. This may prevent unwanted AMPK-mediated Bim expression and apoptosis during transient or physiological bioenergetic stress. [ABSTRACT FROM AUTHOR]