Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An etiological study on renal adenomas with specific references to dysplastic tubular lesions and adenocarcinomas was made, concentrating on histopathological and statistical surveys. Seventy-two unilateral kidneys obtained at random in autopsy cases were examined macro- amd microscopically on the consecutive sliced sections. Adenomas were found frequently in the cortex of 15 cases (20.8%), and particularly dysplastic tubular lesions were considerably associated with adenomas and detected even more frequently in 26 cases (36.2%), whereas fibromas in the medulla of 8 cases (11.1%). Most of the adenomas (86.7%) were found in nephrosclerotic kidneys; i.e., in vascular nephrosclerosis (53.4%), chronic pyelonephritis (13.3%), and in end-stage kidneys. The morphological feature of adenoma cells were also confirmed in the dysplastic tubular epithelial cells. These data imply that long-term renovascular and/or renostromal damages may induce dysplastic tubular lesions and further act as important enhancing or promoting factors on adult renal oncogenesis from the cortical tubular epithelium.
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PMID:An etiological study on renal adenomas: with some references to dysplastic tubular lesions and adenocarcinomas in autopsy and surgery cases. 711 98

Hypersecretion of luteinizing hormone (LH) is implicated in infertility and miscarriages in women. A lack of animal models has limited progress in determining the mechanisms of LH toxicity. We have recently generated transgenic mice expressing a chimeric LH beta subunit (LH beta) in gonadotropes. The LH beta chimera contains the C-terminal peptide of the human chorionic gonadotropin beta subunit. Addition of this peptide to bovine LH beta resulted in a hormone with a longer half-life. Furthermore, targeted expression of the LH beta chimera led to elevated LH levels and infertility in female transgenics. These mice ovulated infrequently, maintained a prolonged luteal phase, and developed pathologic ovarian changes such as cyst formation, marked enlargement of ovaries, and granulosa cell tumors. Testosterone and estradiol levels were increased compared to nontransgenic littermates. An unusual extragonadal phenotype was also observed: transgenic females developed hydronephropathy and pyelonephritis. The pathology observed demonstrates a direct association between abnormal secretion of LH and infertility and underscores the utility of the transgenic model for studying how excess LH leads to cyst formation, ovarian tumorigenesis, and infertility.
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PMID:Targeted overexpression of luteinizing hormone in transgenic mice leads to infertility, polycystic ovaries, and ovarian tumors. 787 75