ABSTRACT
Vein ligation for veno-occlusive erectile dysfunction is being abandoned due to the recurrence rate. Among the reasons for failure is inability to ligate the deep system of veins; the internal pudendal vein. The vein exits the pelvis in the gluteal region, from the lesser sciatic foramen to the greater sciatic foramen, coursing over the ischial spine and sacro-spinous ligament, under the gluteus maximus. This work aims to verify feasibility of the first surgical procedure to ligate the internal pudendal vein through the gluteal approach. This cadaveric study involved five formalin-fixed cadavers. A surface anatomical landmark was designed to identify the ischial spine, at the intersection of two lines: a vertical line from posterior superior iliac spine to ischial tuberosity, and a horizontal line extending from sacro-coccygeal joint, laterally. An incision is cut encompassing the target point. Subcutaneous fat is dissected down to the gluteus maximus, which is split along the direction of its fibers. The vein can be found crossing over the ischial spine. "Shaeer's Vein Ligation - I" appears to be surgically feasible. A protocol for a surgical study is registered at clinicaltrials.gov, and is open for participation.
ABSTRACT
Myocardial ischemiareperfusion injury (MI/R) is considered a main risk factor for global cardiac mortality and morbidity, for which no effective treatment exists. Both inflammation and epigenetic regulation play a pivotal role in the early stage of MI/R. The present study aimed at investigating the prospective anti-inflammatory role of trans-anethole (TNA) in targeting MI/R and its related mechanism in upregulating the expression of the inflammatory and cardiac-related gene (VAV3), and its epigenetic regulators (lncRNA-JRKL-AS1 and miR-1298) that were retrieved from in-silico data analysis in an ischemia/reperfusion (I/R) rat model. MATERIALS & METHODS: TNA was administered in 3 doses (50, 100, and 200 mg/kg), 15 min prior to coronary ligation in male Wistar rats. The left ventricular end-diastolic pressure and dP/dtmax were assessed. Histopathological, biochemical, and molecular analyses were performed to assess the effects of TNA pre-treatment on the I/R rats model. RESULTS: TNA alleviated the I/R-induced cardiac injury pathologically and improved the cardiac function tests and enzymes. At the molecular level, TNA upregulated the expression level of the retrieved RNA-based panel (VAV3 mRNA/miR-1298/lncRNA JRKL-AS1). At the protein level, TNA decreased the cardiac content of the pro-inflammatory cytokine TNF-α. CONCLUSION: TNA has demonstrated a potential ability to alleviate the cardiac injury and attenuate the inflammatory response following ischemia-reperfusion in the rat model through modulation of the expression of RNA panel (VAV3 mRNA/miR-1298/lncRNA JRKL-AS1) and TNF- α protein.
