Bronchogenic cyst with atypical imaging findings and repeated ruptures in a short period of time: A case report.

Bronchogenic cysts are the most common primary cysts of the mediastinum. Although most are asymptomatic, some bronchogenic cysts cause symptoms such as chest pain and dyspnea. Here, we report a case of bronchogenic cyst that ruptured twice in a short period of time in a patient who presented with sudden back pain. The lesion was apparent on computed tomography (CT) as a mass lesion with heterogeneous and high attenuation in the posterior mediastinal region. CT-guided puncture performed for diagnostic purposes revealed the contents as bloody fluid. The patient suffered chest pain approximately 3 months after the first presentation, and re-growth and re-rupture of the mass was suspected. The lesion was surgically resected and pathologically diagnosed as a bronchogenic cyst. Spontaneous rupture is a very rare complication of bronchogenic cyst, usually into the trachea, pleural cavity, or pericardial cavity. However, there are no reports of multiple ruptures. This case highlights the importance of recognizing the atypical imaging findings of bronchogenic cyst and the rare complication of rupture.

[Endosaccular embolization of an intrasellar aneurysm with hypopituitarism: case report].

An 81-year-old male presented with weight loss and hyponatremia. A baseline endocrinological examination revealed anterior pituitary dysfunction. A computed tomography and MRI revealed a large, unruptured intrasellar aneurysm protruding from the right internal carotid artery and pushing the pituitary stalk leftward. The patient developed polyuria and polydipsia from 10 days after commencing corticosteroid supplementation and was diagnosed with partial central diabetes insipidus (DI). Balloon assisted endosaccular embolization was performed about one month after the posterior pituitary dysfunction was identified. The unruptured aneurysm was successfully embolized with Guglielmi detachable coils (GDCs) without narrowing of the parent vessel. DI resolved completely and the posterior pituitary dysfunction improved soon after endosaccular embolization. The remission of DI after coil embolization suggested that the DI might have been induced by the progressive mass effect of the aneurysm rather than by the steroid. An endocrinological evaluation and cerebral angiography confirmed partial recovery of anterior pituitary dysfunction and almost complete obliteration of the aneurysm, respectively at 1 year after the operation. We report a case of hypopituitarism secondary to the large intrasellar aneurysm. This aneurysm was embolized with GDCs, resulting in partial recovery of anterior pituitary dysfunction and complete recovery of posterior pituitary dysfunction.

Role of urotensin II in peripheral tissue as an autocrine/paracrine growth factor.

Urotensin II (UII), originally isolated from goby urophysis, has been shown to be an endogenous ligand for an orphan G-protein-coupled receptor, GPR14. Recent development of PCR quantitative method revealed that UII and UT receptor (GPR14) were expressed in a broad range of tissues and organs, including cardiovascular and renal system, and assumed to function as an autocrine/paracrine factor. UII is a potent vasoconstrictor peptide, whose potency is greater than any other vasoconstrictors thus far known. However, its physiological roles have been found to extend far beyond the regulation of vascular tone. In this review, we focused on the mitogenic action of UII and discuss its underlying cellular mechanisms and potential physiological/pathophysiological role in various human diseases.

Urotensin II is an autocrine/paracrine growth factor for the porcine renal epithelial cell line, LLCPK1.

Urotensin-II (UII), a cyclic dodecapeptide with potent cardiovascular effects, has recently been shown to be abundantly expressed in the human kidney and excreted in human urine. To investigate whether UII acts as an autocrine/paracrine growth factor for renal epithelial cells, we have studied the effects of human UII (hUII) on DNA synthesis, cytosolic free Ca(2+) concentration ([Ca(2+)](i)), ERK activation, and protooncogene (c-myc) expression in a porcine renal epithelial cell line (LLCPK1). hUII stimulated [(3)H]thymidine uptake into quiescent cells in a dose-dependent manner (10(-9) to 10(-7) M); this effect was inhibited by a protein kinase C inhibitor (GF109203X), a MAPK kinase inhibitor (PD98059), and a calcium channel blocker (nicardipine). Neither phosphatidyl inositol-3 kinase inhibitors (LY294002, wortmannin) nor p38 kinase inhibitor (SB203580) affected the hUII-induced DNA syntheses. hUII rapidly (within 5 min) and dose-dependently (10(-9) to 10(-7) M) increased [Ca(2+)](i) in fura-2-loaded cells. hUII also caused a rapid and transient activation of ERK1/2 and induction of c-myc. LLCPK1 cells expressed UII mRNA and its receptor GPR14 mRNA, as determined by RT-PCR, and released UII-like immunoreactivity into media. Neutralization of endogenous UII by anti-hUII antibody, but not nonimmune serum, significantly suppressed DNA synthesis. These data suggest that hUII is an autocrine/paracrine growth factor for renal epithelial cells via activation of both protein kinase C and ERK1/2 pathways as well as Ca(2+) influx via voltage-dependent Ca(2+) channels.

Coexpression of calcitonin receptor-like receptor and receptor activity-modifying protein 2 or 3 mediates the antimigratory effect of adrenomedullin.

Three isoforms of the receptor activity-modifying protein (RAMP) are thought to transport the calcitonin receptor-like receptor (CRLR) to the plasma membrane to function as calcitonin gene-related peptide or adrenomedullin receptors, but their role remains largely unknown. We investigated whether coexpression of RAMP and CRLR are involved in the regulation of cell migration using a monolayer-wounding protocol. Quantification of gene transcripts revealed expression of all RAMP isoforms and CRLR in cultured rat vascular smooth muscle cells (VSMCs), RAMP2 and RAMP3 in rat endothelial cells, and RAMP1 in rat fibroblasts. CRLR expression was minimal in endothelial cells and fibroblasts. Adrenomedullin potently suppressed the migration of VSMCs, whereas calcitonin gene-related peptide did not suppress migration in any cell type. The antimigratory effect of adrenomedullin on VSMCs was potentiated by transfecting CRLR cDNA. Cotransfection of RAMP2 or RAMP3 with CRLR into VSMCs resulted in a slower migratory rate, and this effect was enhanced by adrenomedullin. Migration of fibroblasts was also suppressed after cotransfection of RAMP2 or RAMP3 with CRLR. cAMP agonists had no effect on VSMC migration, and a cAMP antagonist failed to abrogate the antimigratory effect of adrenomedullin. Thus, coexpression of CRLR and RAMP2 or RAMP3 mediates the inhibitory effect of adrenomedullin on cell migration, independent of cAMP-dependent signaling pathways.