Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Indomethacin inhibits prostaglandin synthesis and interferes with renin release; these effects were studied in rabbit renovascular hypertension. 2. Ten intravenous injections (3 mg day-1 kg-1 after two initial doses of 9 mg/kg) of indomethacin were given daily to ten normal rabbits, ten rabbits with two-kidney Goldblatt hypertension (2KH), tension (1KH). Twelve appropriate control rabbits received diluent phosphate buffer without indomethacin. Plasma renin activity and plasma prostaglandin E2 were measured by radioimmunoassay. 3. In the normal group, indomethacin significantly decreased plasma prostaglandin E2 (1-15 to 0-2 ng/ml, SEM 0-2; P less than 0-01) and plasma renin activity (20 to 3 ng h-1 ml-1, SEM 1, P less than 0-01). Plasma creatinine increased slightly but the mean blood pressure was not significantly changed by indomethacin. 4. Six of ten rabbits with 2KH showed results similar to those in the normal rabbits. In four of ten rabbits in which development of 2KH was accompanied by increments in plasma renin activity (18 to 31-5 ng h-1 ml-1, SEM 3 and 4 respectively; P less than 0-01) and plasma prostaglandin E2 (1-2 to 3-4 ng/ml, SEM 0-2 and 0-4 respectively; P less than 0-05), treatment with indomethacin produced renal failure (plasma creatinine increasing to 7-6 mg/100 ml), oliguria, malignant hypertension (mean blood pressure, 168 mmHg, SEM 7-7) and death within 5 days. 5. In 1KH, indomethacin decreased plasma renin activity and plasma prostaglandin E2, but caused increased mean blood pressure (102 to 121 mmHg, SEM 4 and 6 respectively; P less than 0-01) and decreased renal function (plasma creatinine 0-9 +/- 0-04 to 3-5 +/- 1 mg/100 ml, SEM 0-04 and 1 respectively; P less than 0-01). 6. Aggravation of hypertension was conditioned by pre-existing levels of renal function and, to a lesser extent, by plasma renin activities. 7. These results suggest that prostaglandins exert a protective effect on renal function in renovascular hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of indomethacin in rabbit renovascular hypertension. 107 20

WAGR syndrome is caused by an 11p13 deletion and includes Wilms' tumor, aniridia, genitourinary anomalies and mental retardation. We encountered a case of a dysgerminoma originating in an ectopic ovary in a woman with WAGR syndrome. Our patient was a 24-year-old nulliparous woman who was diagnosed with WAGR syndrome. The patient had undergone left nephrectomy for a Wilms' tumor and postoperative chemotherapy at the age of 7 months. She also had a history of glaucoma surgery in both eyes, and was followed up at the Department of Pediatrics for diabetes mellitus, hypertension, liver dysfunction and hyperuricemia. The patient was investigated for oliguria and had elevated levels of blood urea nitrogen (45 mg/dl) and creatinine (5.4 mg/dl); she was admitted to the hospital with acute renal failure and a computed tomography scan revealed a pelvic tumor with a long axis of 10 cm that was obstructing the right ureter. Following insertion of a ureteral stent, the tumor was removed. The tumor had developed in the retroperitoneal space independent of the ovaries. The right adnexa were normal. The tumor was histopathologically diagnosed as dysgerminoma. Follicles were found in part of the tumor; it was thus hypothesized that the tumor developed from an ectopic ovary. The patient was administered etoposide after surgery, and has been recurrence-free for 4 years since treatment.
Mol Clin Oncol 2016 Nov
PMID:Dysgerminoma developing from an ectopic ovary in a patient with WAGR syndrome: A case report. 2788 34