Ca2+ signaling of endothelial cells plays a critical role in controlling blood flow and pressure in small arteries and arterioles. As the impairment of endothelial function is closely associated with cardiovascular diseases (e.g., atherosclerosis, stroke, and hypertension), endothelial Ca2+ signaling mechanisms have received substantial attention. Increases in endothelial intracellular Ca2+ concentrations promote the synthesis and release of endothelial-derived hyperpolarizing factors (EDHFs, e.g., nitric oxide, prostacyclin, or K+ efflux) or directly result in endothelial-dependent hyperpolarization (EDH). These physiological alterations modulate vascular contractility and cause marked vasodilation in resistance arteries. Transient receptor potential (TRP) channels are nonselective cation channels that are present in the endothelium, vascular smooth muscle cells, or perivascular/sensory nerves. TRP channels are activated by diverse stimuli and are considered key biological apparatuses for the Ca2+ influx-dependent regulation of vasomotor reactivity in resistance arteries. Ca2+- permeable TRP channels, which are primarily found at spatially restricted microdomains in endothelial cells (e.g., myoendothelial projections), have a large unitary or binary conductance and contribute to EDHFs or EDH-induced vasodilation in concert with the activation of intermediate/small conductance Ca2+-sensitive K+ channels. It is likely that endothelial TRP channel dysfunction is related to the dysregulation of endothelial Ca2+ signaling and in turn gives rise to vascular-related diseases such as hypertension. Thus, investigations on the role of Ca2+ dynamics via TRP channels in endothelial cells are required to further comprehend how vascular tone or perfusion pressure are regulated in normal and pathophysiological conditions.

Ca2+ signaling of endothelial cells plays a critical role in controlling blood flow and pressure in small arteries and arterioles. As the impairment of endothelial function is closely associated with cardiovascular diseases (e.g., atherosclerosis, stroke, and hypertension), endothelial Ca2+ signaling mechanisms have received substantial attention. Increases in endothelial intracellular Ca2+ concentrations promote the synthesis and release of endothelial-derived hyperpolarizing factors (EDHFs, e.g., nitric oxide, prostacyclin, or K+ efflux) or directly result in endothelial-dependent hyperpolarization (EDH). These physiological alterations modulate vascular contractility and cause marked vasodilation in resistance arteries. Transient receptor potential (TRP) channels are nonselective cation channels that are present in the endothelium, vascular smooth muscle cells, or perivascular/sensory nerves. TRP channels are activated by diverse stimuli and are considered key biological apparatuses for the Ca2+ influx-dependent regulation of vasomotor reactivity in resistance arteries. Ca2+- permeable TRP channels, which are primarily found at spatially restricted microdomains in endothelial cells (e.g., myoendothelial projections), have a large unitary or binary conductance and contribute to EDHFs or EDH-induced vasodilation in concert with the activation of intermediate/small conductance Ca2+-sensitive K+ channels. It is likely that endothelial TRP channel dysfunction is related to the dysregulation of endothelial Ca2+ signaling and in turn gives rise to vascular-related diseases such as hypertension. Thus, investigations on the role of Ca2+ dynamics via TRP channels in endothelial cells are required to further comprehend how vascular tone or perfusion pressure are regulated in normal and pathophysiological conditions.

BACKGROUND: Aspergillosis infection is associated with high morbidity and mortality in liver transplant recipients. This study investigated the prognosis of liver transplant recipients with a pre-operative treatment for paranasal aspergillosis. METHODS: We collected data from 979 cases of patients who underwent liver transplants at the Samsung Medical Center from May 1996 to Feburary 2010. RESULTS: Eight patients were diagnosed with paranasal aspergillosis after functional endoscopic sinus surgery (FESS), before liver transplantation. In these 8 patients, 7 (87.5%) were male, with a mean age of 55 years. All patients had a hepatitis B virus infection, and 6 patients had hepatocellular carcinoma. The mean days from FESS to liver transplantation was 31 (range, 12~47 days) and anti-fungal agents were not used during these periods. All 8 patients were free from a recurrence of aspergillosis after liver transplantation. CONCLUSIONS: Surgical treatment for paranasal aspergillosis in patients prior to liver transplantation does not induce aspergillosis infection after transplantation.
Aspergillosis ; Carcinoma, Hepatocellular ; Hepatitis B virus ; Humans ; Liver ; Liver Transplantation ; Male ; Prognosis ; Recurrence ; Transplants

BACKGROUND: Aspergillosis infection is associated with high morbidity and mortality in liver transplant recipients. This study investigated the prognosis of liver transplant recipients with a pre-operative treatment for paranasal aspergillosis. METHODS: We collected data from 979 cases of patients who underwent liver transplants at the Samsung Medical Center from May 1996 to Feburary 2010. RESULTS: Eight patients were diagnosed with paranasal aspergillosis after functional endoscopic sinus surgery (FESS), before liver transplantation. In these 8 patients, 7 (87.5%) were male, with a mean age of 55 years. All patients had a hepatitis B virus infection, and 6 patients had hepatocellular carcinoma. The mean days from FESS to liver transplantation was 31 (range, 12~47 days) and anti-fungal agents were not used during these periods. All 8 patients were free from a recurrence of aspergillosis after liver transplantation. CONCLUSIONS: Surgical treatment for paranasal aspergillosis in patients prior to liver transplantation does not induce aspergillosis infection after transplantation.
Aspergillosis ; Carcinoma, Hepatocellular ; Hepatitis B virus ; Humans ; Liver ; Liver Transplantation ; Male ; Prognosis ; Recurrence ; Transplants