American Journal of Biomedical Science & Pharmaceutical Innovation

Rarely Encountered Umbilical Cord Pathologies (Literature Review)

2025-08-18T17:22:25+08:00

This review systematizes current knowledge about umbilical cord abnormalities (UCAs) — a heterogeneous group of anomalies including length abnormalities, number of vessels, attachments, nodes, cysts, and vascular malformations. Based on the analysis of scientific literature (2000–2024), the epidemiological data are presented: UCAs occur in 15–35% of pregnancies, with single umbilical artery (SUA) — in 0.5–5%, velmen insertion — up to 50% in monochorionic twins, and true nodes — in 0.3–1.2%. The review details complications: fetal growth restriction (FGR), chronic and acute hypoxia, antenatal death, risks during childbirth (vascular rupture in vasa praevia, asphyxia). Particular attention is paid to early diagnostic methods: ultrasound with Doppler (blood flow assessment, EAP), color Doppler mapping (Velmen attachment), 3D/4D ultrasound in STIC mode (nodes, spatial anomalies), CTG monitoring. Differentiated management tactics are substantiated: from dynamic observation at low risk to planned cesarean section for vasa praevia or IUGR. It is emphasized that timely diagnostics and an individualized approach reduce perinatal mortality and improve outcomes.

Review of Literature on Epidemiology, Diagnostics, Complications of Umbilical Cord Pathology and Management Tactics

2025-08-18T17:22:26+08:00

Microbial Exploitation of Host Purinergic Signaling: Unraveling Clostridioides difficile's Influence on Adenosine Homeostasis

2025-08-18T17:22:27+08:00

Clostridioides difficile is a prominent pathogen responsible for severe gastrointestinal infections, with its pathogenicity intricately linked to interactions with host cellular mechanisms. This study explores how C. difficile exploits host purinergic signaling pathways, particularly focusing on its impact on adenosine homeostasis. Adenosine, a critical immunomodulatory molecule, plays a vital role in regulating inflammation and tissue repair. We investigate the molecular mechanisms by which C. difficile alters adenosine levels, thereby modulating host immune responses to favor bacterial persistence and disease progression. Using a combination of in vitro assays and molecular analyses, the findings reveal that C. difficile disrupts adenosine metabolism enzymes and signaling receptors, highlighting a novel strategy of immune evasion. Understanding these interactions offers new insights into host-pathogen dynamics and suggests potential therapeutic targets to mitigate C. difficile infections.