Publications by authors named "A G Calder"
Biliary obstruction and cholangiocyte hyperproliferation are important features of cholangiopathies affecting the large extrahepatic bile duct (EHBD). The mechanisms underlying obstruction-induced cholangiocyte proliferation in the EHBD remain poorly understood. Developmental pathways, including WNT signaling, are implicated in regulating injury responses in many tissues, including the liver.
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- A meta-analysis was conducted to evaluate whether psychoplastogens like ketamine and psychedelics increase peripheral BDNF levels in humans, which have been suggested as biomarkers for neuroplasticity.
- The analysis included data from 29 studies and found no significant evidence that these substances elevate peripheral BDNF levels, regardless of various factors such as drug type, dosage, or participant characteristics.
- The findings imply that peripheral BDNF may not be a reliable marker for assessing neuroplasticity changes in humans after psychoplastogen administration, highlighting potential discrepancies between preclinical and human studies.
Background: Psychedelic-assisted therapy (PAT) is permitted in Switzerland under its limited medical use program. Data from patients in this program represent a unique opportunity to analyze the real-world practice of PAT.
Aims: This study compared the subjective effects of lysergic acid diethylamide (LSD) and psilocybin between patients undergoing PAT and healthy volunteers.
Article Synopsis
- Two patients of East African descent have been identified with a novel homozygous variant in the parathyroid hormone receptor type 1 (PTH1R), which is linked to Eiken syndrome features such as brachydactyly and skeletal abnormalities.
- Both patients showed parathyroid hormone resistance, resulting in low calcium and high phosphate levels, which initially pointed to pseudohypoparathyroidism, yet genetic testing confirmed a specific PTH1R mutation.
- Functional analysis revealed that both PTH1R variants caused increased basal cAMP signaling and reduced responsiveness to PTH and PTH-related peptide, indicating a disruption in PTH1R signaling pathways associated with their clinical symptoms.