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Autoimmune Diseases and Molecular Mimicry in Tuberculosis.

Biology (Basel)

December 2024

Department of Mathematics and Computer Science, St. Petersburg State University, St. Petersburg 199034, Russia.

Unlabelled: Comorbidities in tuberculosis patients are increasing annually. Autoimmune pathology may influence the diagnosis and treatment of tuberculosis (TB). However, the molecular mimicry between (Mtb) and human autoantigens is an important provocative factor in the development of autoimmunity on one hand.

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Background: Impaired clearance of amyloid-β protein (Aβ) in the peripheral system is a crucial event in the pathogenesis of sporadic Alzheimer's disease (AD). Dysfunctional monocytes with deficient clearance of Aβ and increased secretion of pro-inflammatory factors in the periphery are considered to contribute to AD development. Multiple studies suggest that IL-4 can inhibit the inflammatory response and enhance the expression and activity of cathepsin protease associated with intracellular clearance of Aβ by monocytes.

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Aβ (amyloid beta) oligomers, the major neurotoxic culprits in Alzheimer's disease, initiate early pathophysiological events, including neuronal hyperactivity, that underlie aberrant network activity and cognitive impairment. Although several synaptotoxic effects have been extensively studied, neuronal hyperexcitability, which may also contribute to cognitive deficits, is not fully understood. Here, we found several adverse effects of in vivo injection of Aβ oligomers on contextual memory and intrinsic properties of CA1 pyramidal neurons.

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Introduction: The reproductive potential of older men is influenced by the androgen deficiency and an increased risk of sperm DNA damage. In addition, with aging, a number of other diseases may have a detrimental effect on spermatogenesis. For this reason, the search for methods for correcting impaired spermatogenesis in men of the older age group is of relevance.

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Enhanced phrenic motor neuron BDNF expression elicited by daily acute intermittent hypoxia is undermined in rats with chronic cervical spinal cord injury.

Respir Physiol Neurobiol

November 2024

Breathing Research and Therapeutics Center, Department of Physical Therapy and McKnight Brain Institute, University of Florida, FL 32610, USA. Electronic address:

Acute intermittent hypoxia (AIH) elicits spinal neuroplasticity and is emerging as a potential therapeutic modality to improve respiratory and non-respiratory motor function in people with chronic incomplete spinal cord injury (SCI). Brain-derived neurotrophic factor (BDNF) is necessary and sufficient for moderate AIH-induced phrenic long-term facilitation, a well-studied form of respiratory motor plasticity. Repetitive daily AIH (dAIH) enhances BDNF expression within the phrenic motor neurons of normal rats, but its effects on BDNF after chronic cervical spinal cord injury (cSCI) are unknown.

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