Alligators were injected intraperitoneally with four different doses (10, 1.0, 0.1, and 0.01 mg/kg body weight) of a mixture of bacterial lipopolysaccharides (LPS) derived from three different types of bacteria (Escherichia coli, Pseudomonas aeruginosa, and Klebsiella pneumoniae). Injection of the alligators with the LPS mixture resulted in a dose- and time-dependent increase in total peripheral leukocytes Lymphocytes increased at days 3 and 4 post-injection, and decreased back to baseline levels at day 7 for all doses. Alligators that were not treated, and those injected with pyrogen-free saline, did not exhibit statistically significant changes in total leukocytes during the course of the study. Injection of alligators with 0.5 mg LPS/kg body weight derived from one of three bacterial species revealed that the leukocyte increases observed were not statistically different for all three types of LPS. The animals displayed the same increases in total counts and the levels of all circulating leukocyte types were not different between animals treated with a combination of LPS from all three bacterial species.
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http://dx.doi.org/10.1016/j.vetimm.2006.01.018 | DOI Listing |
Alzheimers Dement
December 2024
University of Florida College of Medicine, Gainesville, FL, USA.
Background: Peripheral blood mononuclear cells (PBMCs) were obtained from patients across different stages of Parkinson's disease (PD) progression and stimulated ex vivo to develop biomarkers for predicting PD progression.
Method: PBMCs obtained at one time-point from patients with moderate stage PD (>5 years after diagnosis) (n = 30), early stage PD (<5 years after diagnosis) (n = 27), prodromal PD (rapid-eye-movement sleep behavior disorder patients) (n = 14), and healthy controls (HCs) (n = 9) were isolated from whole blood and cryopreserved. Samples were thawed, then pan-monocytes and T-cell populations were isolated from PBMCs and subjected to treatment with vehicle or IFN-γ.
Alzheimers Dement
December 2024
Alzheimer's disease and other cognitive disorders unit, Hospital Clínic, IDIBAPS, Barcelona, Spain.
Background: Sleep-wake alterations are common symptoms in Alzheimer's Disease (AD) associated with faster cognitive decline. Noradrenaline dysfunction and neuroinflammation have been proposed as potential driving mechanisms. The ADIS project aims to study the relationship between sleep-wake patterns, immune signatures (peripheral blood cytotoxic lymphocytes), and noradrenergic markers across the AD spectrum.
View Article and Find Full Text PDFKardiologiia
December 2024
Research Institute of Cardiology, Branch of the Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk.
Aim: Comparative assessment of structural changes in cardiomyocyte mitochondria of the right atrial appendage and the mitochondrial respiratory function in peripheral blood leukocytes in a cohort of patients after acute decompensated heart failure (ADHF) and with stable chronic heart failure of ischemic etiology with reduced ejection fraction (CHFrEF) or moderately reduced ejection fraction (CHFmrEF) of the left ventricle.
Material And Methods: The study analyzed 40 micrographs of right atrial appendage cardiomyocytes obtained from 12 patients with CHFrEF and CHFmrEF. The study protocol was registered on ClinicalTrials.
Alzheimers Dement
December 2024
Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona, Spain.
Background: Leukocyte telomere length (LTL) serves as a proxy for tissue-specific TL and peripheral immune aging. Its association with aging-related brain endophenotypes, cognitive functioning, and Alzheimer's disease (AD) risk is established, but the underlying molecular mechanisms remain elusive. Investigating LTL's association with AD biomarkers is crucial for identifying its role in brain resilience and disease progression.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, San Francisco, San Francisco, CA, USA.
Background: Mitochondrial DNA copy number (mtDNAcn) quantifies the number of mitochondria genomes per nucleated cell, with reduced mtDNAcn being associated with increased Alzheimer's disease (AD) neuropathology. Blood-based mtDNAcn has technical confounders, such as DNA purification, and biological confounders, such as compensatory upregulation of mtDNA. Therefore, we optimized a protocol for mtDNAcn quantification using droplet digital PCR (ddPCR) by testing (i) whole peripheral blood mononuclear cells (PBMCs) vs platelet-depleted PBMCs, (ii) column-based DNA extraction vs cell lysate, and (iii) mitochondrial DNA replication (mtDNArep).
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