Blue Light Does Not Affect Fruit Quality or Disease Development on Ripe Blueberry Fruit During Postharvest Cold Storage

Blueberry fruit are perishable after harvesting due to fruit softening, water loss and susceptibility to pathogens. Light, especially blue light, increases the accumulation of anthocyanins and reduces postharvest decay in some fruits, but the effect of blue light on postharvest fruit quality attributes in blueberries is unknown. In this study, we evaluated the effect of blue light on fruit quality, anthocyanin accumulation and disease development during postharvest cold storage (2 °C–4 °C) in two experiments with southern highbush blueberry ‘Star’ and rabbiteye blueberry ‘Alapaha’. Overall, diurnal blue light did not affect postharvest fruit quality attributes, such as visual defects, fruit compression, skin puncture, total soluble solid content and titratable acidity, in the two cultivars compared with their respective controls (diurnal white light or continuous darkness). Further, there was no effect of blue light on fruit color and anthocyanin accumulation. Fruit disease incidence in ‘Star’ ranged from 19.0% to 27.3% after 21 days and in ‘Alapaha’ from 44.9% to 56.2% after 24 days in postharvest storage, followed by 4 days at room temperature, but blue light had no consistent effect on postharvest disease incidence for either cultivar. Disease progression following artificial inoculations with Alternaria tenuissima and Colletotrichum acutatum in ‘Star’ was not influenced by light treatment prior to inoculation and during fruit storage. In a separate experiment, we tested the effect of blue light on color development in ‘Farthing’, a southern highbush blueberry cultivar with fruit prone to non-uniform ripening, whereby the stem-end remains green as the rest of the fruit turns blue. Although green stem-end spots turned blue over time, there was no statistically significant effect of the blue light treatment. Overall, these data indicate that blue light does not affect fruit quality attributes or disease development in ripe blueberry fruit during postharvest storage in the conditions investigated here

Evaluation of delayed LNFPIII treatment initiation protocol on improving long-term behavioral and neuroinflammatory pathology in a mouse model of Gulf War Illness

Chemical overexposures and war-related stress during the 1990-1991 Gulf War (GW) are implicated in the persisting pathological symptoms that many GW veterans continue to endure. These symptoms culminate into a disease known as Gulf War Illness (GWI) and affect about a third of the GW veteran population. Currently, comprehensive effective GWI treatment options are unavailable. Here, an established GWI mouse model was utilized to explore the (1) long-term behavioral and neuroinflammatory effects of deployment-related GWI chemicals exposure and (2) ability of the immunotherapeutic lacto-N-fucopentaose III (LNFPIII) to improve deficits when given months after the end of exposure. Male C57BL6/J mice (8-9 weeks old) were administered pyridostigmine bromide (PB) and DEET for 14 days along with corticosterone (CORT; latter 7 days) to emulate wartime stress. On day 15, a single injection of the nerve agent surrogate diisopropylfluorophosphate (DFP) was given. LNFPIII treatment began 7 months post GWI chemicals exposure and continued until study completion. A battery of behavioral tests for assessment of cognition/memory, mood, and motor function in rodents was performed beginning 8 months after exposure termination and was then followed by immunohistochemcal evaluation of neuroinflammation and neurogenesis. Within tests of motor function, prior GWI chemical exposure led to hyperactivity, impaired sensorimotor function, and altered gait. LNFPIII attenuated these motor-related deficits and improved overall grip strength. GWI mice also exhibited more anxiety-like behavior that was reduced by LNFPIII; this was test-specific. Short-term, but not long-term memory, was impaired by prior GWI exposure; LNFPIII improved this measure. In the brains of GWI mice, but not in mice treated with LNFPIII, glial activation was increased. Overall, it appears that months after exposure to GWI chemicals, behavioral deficits and neuroinflammation are present. Many of these deficits were attenuated by LNFPIII when treatment began long after GWI chemical exposure termination, highlighting its therapeutic potential for veterans with GWI