Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
Surg Endosc ; 18(10): 1539, 2004 Oct.
Article in English | MEDLINE | ID: mdl-15791386

ABSTRACT

A patient presented with hypertension, hypokalemia, and a 1.2-cm left adrenal tumor. Conn's syndrome was diagnosed, for which laparoscopic adrenalectomy is now the therapy of choice. This case was complicated by an ipsilateral ectopic pelvic kidney. A laparoscopic left adrenalectomy was performed via a lateral transabdominal approach. Without the usual anatomic landmark of the ipsilateral kidney, the left adrenal gland was difficult to identify, so intraoperative ultrasound was used to locate the lesion. Postoperatively, the patient's blood pressure and potassium normalized. This is the first documented report of a laparoscopic adrenalectomy performed for adrenal adenoma with the anatomic disruption of an ipsilateral pelvic kidney.


Subject(s)
Adrenalectomy/methods , Hyperaldosteronism/complications , Hyperaldosteronism/surgery , Kidney/abnormalities , Laparoscopy , Humans , Male , Middle Aged
2.
Proc Natl Acad Sci U S A ; 97(20): 11086-91, 2000 Sep 26.
Article in English | MEDLINE | ID: mdl-10995467

ABSTRACT

A requirement for scaffolding complexes containing internalized G protein-coupled receptors and beta-arrestins in the activation and subcellular localization of extracellular signal-regulated kinases 1 and 2 (ERK1/2) has recently been proposed. However, the composition of these complexes and the importance of this requirement for function of ERK1/2 appear to differ between receptors. Here we report that substance P (SP) activation of neurokinin-1 receptor (NK1R) stimulates the formation of a scaffolding complex comprising internalized receptor, beta-arrestin, src, and ERK1/2 (detected by gel filtration, immunoprecipitation, and immunofluorescence). Inhibition of complex formation, by expression of dominant-negative beta-arrestin or a truncated NK1R that fails to interact with beta-arrestin, inhibits both SP-stimulated endocytosis of the NK1R and activation of ERK1/2, which is required for the proliferative and antiapoptotic effects of SP. Thus, formation of a beta-arrestin-containing complex facilitates the proliferative and antiapoptotic effects of SP, and these effects of SP could be diminished in cells expressing truncated NK1R corresponding to a naturally occurring variant.


Subject(s)
Apoptosis/drug effects , Apoptosis/physiology , Arrestins/physiology , Receptors, Neurokinin-1/physiology , Signal Transduction/drug effects , Substance P/pharmacology , Animals , Cell Division/drug effects , Cell Division/physiology , Cell Line , MAP Kinase Signaling System , Rats , beta-Arrestins
SELECTION OF CITATIONS
SEARCH DETAIL
...