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Biomarkers.

Alzheimers Dement

December 2024

All India Institute of Medical Sciences, New Delhi, India.

Background: Recent research on Alzheimer's disease (AD) has highlighted that the oxidative damage is the earliest event of disease. These oxidative modifications are closely associated with inflammatory molecules. It is necessary to explore these two pathways with AD pathophysiology and targeted for therapeutic intervention.

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Loss-of-function GHSR variants are associated with short stature and low IGF-I.

J Clin Endocrinol Metab

January 2025

Division of Pediatric Endocrinology, Department of Pediatrics, Willem-Alexander Children's Hospital, Leiden University Medical Centre, Leiden, The Netherlands.

Context: The growth hormone (GH) secretagogue receptor, encoded by GHSR, is expressed on somatotrophs of the pituitary gland. Stimulation with its ligand ghrelin, as well as its constitutive activity, enhances GH secretion. Studies in knock-out mice suggest that heterozygous loss-of-function of GHSR is associated with decreased GH response to fasting, but patient observations in small case reports have been equivocal.

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Background: Alzheimer's disease (AD), the most common type of dementia, affects at least twenty-four million people globally, yet, the causation, mechanisms of progression, and therapeutic strategies remain elusive. Currently, tRNA-derived RNA fragments (tRFs), a family of recently discovered small non-coding RNAs (sncRNAs), have surfaced as promising biomarkers for many diseases, including AD. Our work revealed that several AD-impacted tRFs in human hippocampus, CSF, and serum.

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Background: Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Dysfunction of mitochondria and oxidative stress are known to aggravate the disease pathology. Sirtuins, NAD-dependent deacetylases, have a well-defined role in this pathway and thus can serve as a potential biomarker for the early detection of the disease.

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Bronchopulmonary dysplasia, the most prevalent chronic lung disease of prematurity, is often treated with glucocorticoids (GCs) such as dexamethasone (DEX), but their use is encumbered with several adverse somatic, metabolic, and neurologic effects. We previously reported that systemic delivery of the GC prodrug ciclesonide (CIC) in neonatal rats activated glucocorticoid receptor (GR) transcriptional responses in lung but did not trigger multiple adverse effects caused by DEX. To determine whether limited systemic metabolism of CIC was solely responsible for its enhanced safety profile, we treated neonatal rats with its active metabolite desisobutyryl-ciclesonide (Des-CIC).

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