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Lenhart, P.

Publications and source records attributed to Lenhart, P..

2 recordsLinked to original sources

Advancing the design of the kissing bug kill trap for surveillance of triatomines

Standardized surveillance and control of kissing bugs (Hemiptera: Reduviidae: Triatominae), the insect vectors of the Chagas disease parasite Trypanosoma cruzi, which causes Chagas disease, remains difficult. The Kissing Bug Kill Trap consists of solar powered LED lights mounted over a column of black funnels. It operates autonomously to capture, kill and preserve adult triatomines. We conducted experiments from 2022-2024 testing potential ways to improve trap performance, ease of deployment, and minimize cost. Thirteen prototypes evaluated in Texas, Guatemala, and Mexico captured 1,531 triatomines. In 2022-2023 we selected a six-funnel trap suspended from a single support pole with an angle bracket, and with four LED lights and a solar panel mounted above the rain-guard, as a reference trap. In 2023, traps with smaller funnels, blue funnels, and blue lights were inferior to the reference trap based on high by-catch of other arthropods and/or fewer triatomines caught per day. In 2024, traps with more or fewer than six funnels or with LED lights mounted on or below the rain guard did not outperform the reference trap. The experiments added five new triatomine species to the four already known to be caught by the Kissing Bug Kill Trap and revealed differences and similarities in phenology of dispersal flights of Triatoma gerstaeckeri over a three-year period in Texas. The reference trap was selected as the pre-commercial prototype, based on its suitability for triatomine surveillance and potential for reducing the risk of T. cruzi infection by intercepting dispersing adult triatomines before they reach human habitats.

ecology↗

Traumatic Brain Injury Exacerbates Alzheimer's Disease Pathology in the Retinas of TgF344-AD Rats

Alzheimers disease (AD) is a neurodegenerative condition that affects 6.2 million people age 65 and older in the U.S. alone, and is the leading cause of dementia. Moreover, AD can lead to visual impairment, and AD histopathology also manifests in the retina. However, the factors that modulate AD pathophysiology and lead to varied susceptibility and presentation in the population are not well understood. In this context, traumatic brain injury (TBI), which can arise from sport concussions, military combat, and other causes, is associated with a 2.3-fold higher risk of developing AD and AD-related dementias (ADRD). Thus, we set out to evaluate the effects of TBI, AD, and their combination, on retinal histopathology. Several animal models have been developed to investigate the mechanisms underlying AD, but many have been limited by imperfect recapitulation of human pathology, and no model of TBI-associated AD (AD-TBI) has been characterized. To address this gap, we generated an innovative model of AD-TBI by taking advantage of a transgenic rat model (Tg-F344-AD) shown to recapitulate the main features of human AD pathology, and combining it with a twotime unilateral controlled cortical impact paradigm to mimic repetitive mild TBI (rmTBI). Histopathological analyses at four months post-impact confirm the presence of AD markers in transgenic retinas, and an increased severity of AD pathology due to TBI. Together, these results contribute to our understanding of the effects of TBI on AD retinopathy, with implications for patient care and therapeutic development.

neuroscience↗