Wild rats ( spp.) carry many zoonotic pathogens including Due to the close proximity of rats to humans in urban environments, the potential for disease transmission is high. is a protozoan parasite which when ingested causes serious human illness. Despite its importance, genetic characterization of in wild rats in the Hainan province of China has not been performed. In this study, we analyzed the occurrence and genetics of in wild rats from Hainan, China. From December 2017 to October 2018, 150 wild rats were captured and fresh fecal material was collected from intestinal sections. Rat species were identified by PCR-based amplification and analysis of the vertebrate cytochrome () gene. was examined by PCR amplification of the partial small subunit of ribosomal DNA (SSU rDNA). were subtyped by PCR analysis of the gp60 gene. A total of four rat species were identified including Asian house rats () (n = 46), brown rats () (n = 56), Edward's long-tailed rats () (n = 38) and muridae () (n = 10), with positive rates of 73.9%, 28.6%, 55.3% and 40.0%, respectively (average infection rate: 50.0%, 75/150. Sequence analysis confirmed the presence of four species and two genotypes including (n = 11); (n = 2); (n = 1); and (n = 1); rat genotypes III (n = 13) and IV (n = 47). Three novel subtypes of were identified in 6 of the 11 infected Edward's long-tailed rats: XVcA2G1a (n = 4), XVcA2G1b (n = 1) and XVdA3 (n = 1). The identification of human pathogenic and zoonotic , and suggested that wild rats infected with pose a threat to human health. Taken together, these findings highlight the need to control the rat population in Hainan, China. The need to improve the public awareness of the risk of disease transmission from wild rats to humans is also highlighted.
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http://dx.doi.org/10.1016/j.ijppaw.2019.03.017 | DOI Listing |
Alzheimers Dement
December 2024
Department of Neurology, University of Colorado Alzheimer's and Cognition Center, and the Linda Crnic Institute for Down Syndrome, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
Background: Increasing age is the greatest risk factor for age-associated cognitive decline (AACD) and, especially in females, for developing Alzheimer's disease (AD). Mechanisms underlying this connection are unknown, but neuronal loss and brain atrophy accompany aging and AD and likely contribute to cognitive deficits. There are currently no means to measure neuronal cell death during life and no means to prevent it.
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December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Background: Imaging biomarkers have helped to reconceptualize Alzheimer's disease pathophysiology. More specifically, positron emission tomography (PET) radiopharmaceuticals for non-invasively assessing amyloid-beta (Aβ) plaques, glucose metabolism, and glial reactivity allow for tracking disease progression in a temporally ordered manner. However, whether transgenic models recapitulate biomarker-related changes remains elusive.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Background: Imaging biomarkers have helped to reconceptualize Alzheimer's disease pathophysiology. More specifically, positron emission tomography (PET) radiopharmaceuticals for non-invasively assessing amyloid-beta (Aß) plaques, glucose metabolism, and glial reactivity allow for tracking disease progression in a temporally ordered manner. However, whether transgenic models recapitulate biomarker-related changes remains elusive.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: Recent studies have suggested a transient glucose hypermetabolism in early phases of Alzheimer's Disease (AD), which is followed by a characteristic glucose hypometabolism in dementia stages. This phenomenon desveres further investigation and it is suggested to be associated to glial/inflammatory or compensatory neuronal responses. Here, we aimed to longitudinally investigate brain glucose metabolism in an AD animal model and explore associated cellular and inflammatory changes.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is a neurodegenerative disorder without a cure. Targeting this multifactorial disease by repurposing FDA approved drugs serves as a faster mode of treatment due to its pre-established human safety. We tested terazosin (TZ), an a-1 adrenergic receptor (AR) antagonist and phosphoglycerate kinase-1 (PGK1) activator as having potential to treat AD.
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