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The Asian longhorned tick, Haemaphysalis longicornis, an invasive species associated with human pathogens, has spread rapidly across the eastern USA. Questing H. longicornis ticks recovered from active surveillance conducted from 1 May to 6 September, 2019 throughout Pennsylvania were tested for rickettsial pathogens. Of 265 ticks tested by PCR for pathogens, 4 (1.5%) were positive for Anaplasma phagocytophilum. Sequence analysis of the 16S rRNA gene confirmed two positives as A. phagocytophilum–human agent variant. This is the first reported detection of A. phagocytophilum–human pathogenic strain DNA in exotic H. longicornis collected in the USA. [ABSTRACT FROM AUTHOR]

This document is an abstract from the Journal of Clinical & Translational Science. It includes three separate studies. The first study aims to identify candidate variants that cause sudden arrhythmic death (AN-SAD) in racehorses. Whole genome sequencing was performed on AN-SAD cases and controls, and variants were selected based on case-control analysis. The second study investigates the effects of ketamine on brain-derived neurotrophic factor (BDNF) levels in the corticoaccumbens circuit of rats. Results show that repeated ketamine administration increases BDNF levels in the nucleus accumbens. The third study explores the role of bHLHe40 in systemic sclerosis-associated pulmonary fibrosis. It is found that bHLHe40, TLL1, and LOX-PP may serve as targets for therapeutic intervention in stopping the progression of pulmonary fibrosis. [Extracted from the article]

We collected questing Haemaphysalis longicornis ticks from southeastern counties of Pennsylvania, USA. Of 263 ticks tested by PCR for pathogens, 1 adult female was positive for Borrelia burgdorferi sensu stricto, yielding a 0.4% infection rate. Continued monitoring of this invasive tick is essential to determine its public health role. [ABSTRACT FROM AUTHOR]

Wildlife reintroductions to peopled landscapes pose socio-ecological opportunities and risks, and a responsibility to people as well as wildlife. Human–wildlife conflicts can escalate rapidly where anthropogenic foods and feeding cause wildlife to congregate and damage property. Those conflicts polarise attitudes to the wildlife and may cascade into conflicts between people over wildlife. The native parrot, kākā (Nestor meridionalis), was reintroduced to Wellington City in 2002 and we suspect that it initiated a classical human–wildlife conflict cascade. We tested for feeding-induced damage, and different attitude scores amongst neighbours using a postal household survey. We received 313 completed surveys, a 55.9% response rate, across eight suburbs. Minor to severe damage, costing up to NZ$3000 to repair, was reported to trees, buildings, and outdoor furniture. Seventeen respondents reported feeding kākā, mostly fruit and vegetables, but also sugar water, bread, and nuts and seeds, and we received surveys from 33 of their non-feeding neighbours. Feeding significantly increased reports of kākā, and kākā abundance was positively associated with kākā damage. Neighbourhoods closer to Zealandia (the wildlife sanctuary where kākā are fed) and the neighbours of people who fed kākā were statistically more likely to incur property damage than more distant suburbs and residents. Neighbours' attitudinal scores about kākā and native birds were significantly negatively associated with greater kākā damage. The reintroduction of kākā has initiated a feeding-induced wildlife–human conflict. We discuss what can be learned from the experience with kākā in Wellington City for urban wildlife conservation in the future. The reintroduction and feeding of kākā (Nestor meridionalis) in Wellington City, New Zealand, initiated a human–wildlife conflict. Feeding increases damage by kākā and caused attitudes to the birds amongst neighbours to diverge. The human dimensions of wildlife reintroductions, especially to cities, require greater pre-emptive consideration. [ABSTRACT FROM AUTHOR]

A non-synonymous single nucleotide polymorphism of the human serotonin 5-HT2C receptor (5-HT2CR) gene that converts a cysteine to a serine at amino acid codon 23 (Cys23Ser) appears to impact 5-HT2CR pharmacology at a cellular and systems level. We hypothesized that the Cys23Ser alters 5-HT2CR intracellular signaling via changes in subcellular localization in vitro. Using cell lines stably expressing the wild-type Cys23 or the Ser23 variant, we show that 5-HT evokes intracellular calcium release with decreased potency and peak response in the Ser23 versus the Cys23 cell lines. Biochemical analyses demonstrated lower Ser23 5-HT2CR plasma membrane localization versus the Cys23 5-HT2CR. Subcellular localization studies demonstrated O-linked glycosylation of the Ser23 variant, but not the wild-type Cys23, may be a post-translational mechanism which alters its localization within the Golgi apparatus. Further, both the Cys23 and Ser23 5-HT2CR are present in the recycling pathway with the Ser23 variant having decreased colocalization with the early endosome versus the Cys23 allele. Agonism of the 5-HT2CR causes the Ser23 variant to exit the recycling pathway with no effect on the Cys23 allele. Taken together, the Ser23 variant exhibits a distinct pharmacological and subcellular localization profile versus the wild-type Cys23 allele, which could impact aspects of receptor pharmacology in individuals expressing the Cys23Ser SNP. [ABSTRACT FROM AUTHOR]